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"Kanker paru merupakan salah satu jenis kanker mematikan dengan terjadinya kasus paling banyak di dunia. Mutasi gen yang terjadi pada sel organ paru menjadi penyebab utama terjadinya kanker paru. Salah satu gen yang berpengaruh terhadap pembelahan sel kanker, yaitu ferritin mitokondria (FTMT). Mekanisme yang diatur oleh gen FTMT yaitu dengan memodulasi metabolisme zat besi (Fe2+) didalam mitokondria yang diinduksi oleh adanya stres oksidatif. Mekanisme yang diatur oleh gen FTMT dengan jumlah ekspresi yang tinggi akibat adanya stres oksidatif berupa H2O2 didalam sel kanker. Senyawa stres oksidatif berupa H2O2 merupakan senyawa toksik yang dapat menghasilkan Reactive Oxygen Spesies (ROS) dan berperan penting dalam proses pengaturan sistem fisiologis dalam sel. Reactive Oxygen Spesies (ROS) yang dihasilkan dengan jumlah tinggi akan mengarah ke mekanisme kematian sel (ferroptosis). Penelitian ini bertujuan untuk mengetahui ekspresi gen FTMT dan viabilitas sel pada cell line A549 (non-small cell lung carcinoma) yang diinduksi oleh senyawa H2O2 sebagai stres oksidatif dengan perlakuan berbagai konsentrasi, yaitu 50 μM, 100 μM, 150 μM, 200 μM, dan 300 μM dengan menggunakan metode qRT-PCR. Hasil penelitian ini menunjukkan peningkatan ekspresi gen FTMT dan penurunan viabilitas sel secara signifikan pada perlakuan H2O2 dengan rentang konsentrasi 50 μM sampai 100 μM. Dengan demikian, perlakuan stres oksidatif H2O2 mempunyai peran penting dalam meregulasi gen FTMT yang berkaitan dengan morfologi dan viabilitas sel A549 kanker paru.

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Lung cancer is a type of deadly cancer with the most cases occurring in the world. Gene mutations that occur in lung organ cells are the main cause of lung cancer. One of the genes that influences cancer cell division is mitochondrial ferritin (FTMT). The mechanism regulated by the FTMT gene is by modulating iron (Fe2+) metabolism in mitochondria which is induced by oxidative stress. The mechanism regulated by the FTMT gene with high levels of expression is due to oxidative stress in the form of H2O2 in cancer cells. Oxidative stress compounds in the form of H2O2 are toxic compounds that can produce Reactive Oxygen Species (ROS) and play an important role in the process of regulating physiological systems in cells. Reactive Oxygen Species (ROS) produced in high amounts will lead to a cell death mechanism (ferroptosis). This study aims to determine the expression of the FTMT gene and cell viability in the A549 (non-small cell lung carcinoma) cell line which was induced by H2O2 compounds as oxidative stress with various concentrations of treatment, namely 50 μM, 100 μM, 150 μM, 200 μM, and 300 μM using the qRT-PCR method. The results of this study showed an increase in FTMT gene expression and a significant decrease in cell viability in H2O2 treatment with a concentration range of 50 μM to 100 μM. Thus, H2O2 oxidative stress treatment has an important role in regulating the FTMT gene which is related to the morphology and viability of lung cancer A549 cells."

"Gen EHMT2 dapat meregulasi metilasi protein histon yang berdampak pada disregulasi epigenetik dan terganggunya proses transkripsi. Hal tersebut dapat menjadi faktor yang memengaruhi metastasis tumor pada kanker paru. Salah satu inhibitor spesifik yang dapat digunakan untuk menghambat aktivitas dan menurunkan ekspresi gen EHMT2 adalah BIX01294. Sejauh ini, konsentrasi inhibitor BIX01294 yang digunakan untuk penelitian ekspresi gen EHMT2 pada kanker paru berkisar pada 2–10 μM. Oleh karena itu, perlu dilakukan penelitian lanjutan terkait efektivitas inhibitor BIX01294 untuk menurunkan ekspresi gen EHMT2 dengan konsentrasi >10 μM. Penelitian ini bertujuan untuk mengetahui efektivitas dari inhibitor BIX01294 dalam menurunkan ekspresi gen EHMT2 pada sel kanker paru A549 melalui empat konsentrasi inhibitor yang berbeda, yakni 12,5 μM, 15 μM, 17,5 μM, dan 20 μM. Metode yang digunakan adalah RT-qPCR. Hasil penelitian menujukkan bahwa inhibitor BIX01294 dapat memengaruhi konfluensi dan viabilitas sel kanker paru A549. Sampel sel kanker paru A549 yang tidak diberi perlakuan dengan inhibitor BIX01294 memiliki konfluensi sel dan nilai viabilitas yang lebih tinggi dibandingkan dengan sampel seri inhibitor BIX01294. Selain itu, inhibitor BIX01294 juga dapat menurunkan ekspresi gen EHMT2 sel kanker paru A549 secara dose - dependant . Dengan demikian, dapat disimpulkan bahwa inhibitor BIX01294 dengan konsentrasi 12,5 μM; 15 μM; 17,5 μM; dan 20 μM dapat menurunkan ekspresi gen EHMT2 dan viabilitas pada sel kanker paru A549 secara dose-dependant.

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The EHMT2 gene has the ability to control the methylation of histone proteins, which can lead to disruptions in epigenetic regulation and the transcription process. This can be a factor influencing tumor metastasis in lung cancer. A specific EHMT2 gene inhibitor, BIX01294, has been identified as an effective agent in inhibiting the activity of the EHMT2 gene. Previous research on lung cancer used BIX01294 concentrations between 2–10 μM. As a result, additional studies are needed to evaluate the efficacy of the BIX01294 inhibitor in reducing EHMT2 gene expression at concentrations greater than 10 μM. The objective of this study is to evaluate the potency of the BIX01294 inhibitor in reducing EHMT2 gene expression within A549 lung cancer cells at four different concentrations: 12.5 μM, 15 μM, 17.5 μM, and 20 μM. The method used in this study is RT-qPCR. The study’s findings reveal that the BIX01294 inhibitor can impact the confluence and viability of A549 lung cancer cells. The A549 lung cancer cell samples that were not subjected to the BIX01294 inhibitor exhibited higher cell confluence and viability values compared to those that were treated with the inhibitor. Furthermore, the BIX01294 inhibitor can also decrease the expression of the EHMT2 gene in A549 lung cancer cells in a dose-dependent manner. Therefore, it can be concluded that the BIX01294 inhibitor, at concentrations of 12.5 μM, 15 μM, 17.5 μM, and 20 μM, demonstrates a dose-dependent reduction in EHMT2 gene expression and the viability of A549 lung cancer cells."

"Kanker paru merupakan penyebab utama keganasan di dunia. Kanker paru memiliki insidensi dan angka kematian yang cukup besar pada populasi laki-laki maupun perempuan. Diperlukan metode diagnosis dan pemantauan terapi yang efektif untuk mengatasi masalah kanker paru di dunia. Penelitian ini merupakan studi eksperimental secara in vitro dengan sel A549. Kultur sel A549 ditumbuhkan dalam medium DMEM lalu diekstraksi dengan RIPA buffer. Sel A549 dengan dan tanpa pemberian doxorubicin, serta sel normal dibuat masing-masing sebanyak 4 sampel dan dianalisis menggunakan Differential Scanning Calorimetry (DSC). Hasil analisis profil termogram DSC yang didapatkan berupa titik lebur dan entalpi lebur. Rata-rata titik lebur dan entalpi lebur dari tiap sampel dianalisis secara statistik menggunakan uji Anova satu arah dilanjutkan dengan uji post-hoc bonferroni. Penelitian ini menunjukkan adanya perbedaan bermakna rata-rata titik lebur antara sel normal dan sel A549 serta antara sel A549 dan sel A549 dengan pemberian doxorubicin. Berdasarkan hasil ini, DSC memiliki potensi untuk digunakan sebagai alat diagnosis dan pemantauan terapi kanker paru.

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Lung cancer is the major cause of malignancy in the world. Lung cancer has significant incidence and mortality rate in both male and female populations. An effective method of diagnosis and monitoring therapy is needed to overcome lung cancer problems in the world. This research is an experimental in vitro study with A549 cell line. A549 cell culture was grown in DMEM medium and extracted with RIPA buffer. A549 cells with and without doxorubicin treatment, and normal cell, were prepared 4 samples each and analyzed using Differential Scanning Calorimetry (DSC).

The results of the DSC thermogram profiling obtained in the form of melting point and enthalpy. The average melting point and enthalpy of each sample were analyzed statistically using one-way ANOVA test followed by Bonferroni post-hoc test. This study showed a significant difference in the average melting point between normal cell and A549 cell, also between A549 cell and A549 cell with doxorubicin treatment. Based on these results, DSC has the potential to be used as a diagnostic and therapeutic monitoring tool for lung cancer."

"Pendahuluan: Endometriosis merupakan suatu kelainan jinak ginekologi yang dapat mengalami transformasi menjadi kanker. Stres oksidatif diduga berperan dalam perkembangan penyakit endometriosis. Gen supresor tumor ARID1A banyak ditemukan termutasi dan inaktif pada kanker ovarium yang berhubungan dengan endometriosis. Tujuan penelitian adalah untuk menganalisis peran stres oksidatif terhadap ekspresi gen supresor tumor ARID1A dalam transformasi endometriosis menjadi ganas. Metoda: Penelitian dimulai dengan 10 sampel jaringan kanker ovarium, 10 sampel endometriosis dan3 jaringan endometrium eutopik sebagai kontrol yang diisolasi mRNA dan proteinnya. Analisis ekspresi gen ARID1A pada tingkat mRNA dilakukan dengan pemeriksaan RT-qPCR dan pada tingkat protein dengan ELISA. Pada sel endometriosis dan kanker ovarium dilakukan analisis stres oksidatif dengan pemeriksaan aktivitas antioksidan MnSOD dan pemeriksaan kadar MDA sebagai salah bukti kerusakan salah satu komponen sel. Setelah itu dilakukan uji eksperimental pada kultur sel endometriosis dan endometrium eutopik sebagai kontrol. Kedua sel kultur diinduksi dengan H2O2 konsentrasi 0 nM, 100 nM, dan 1000 nM. Analisis dilakukan terhadap ketahanan hidup sel, kadar ROS dan ekspresi gen ARID1A pada tingkat mRNA dan protein. Hasil: Efek induksi H2O2 dalam menekan ekspresi gen ARID1A sel endometriosis dan sel endometrium eutopik pada tingkat mRNA dan protein, bermakna, meskipun pada kanker ovarium tidak bermakna pada penelitian ini. Kesimpulan: Stres oksidatif berperan dalam menekan ekspresi gen supresor tumor ARID1A ditingkat mRNA dan protein pada endometriosis.

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Introduction: Endometriosis as a gynecologic benign lesion, can transform itself into cancer. Oxidative stress is considered as an important factor in endometriosis development. Studies found that ARID1A as tumor suppressor gene, was frequently mutated and inactivated in endometriosis associated ovarian cancer. The aim of the study is to analyze the role of oxidative stress on ARID1A expresion in endometriosis malignant transformation.

Methods: This study started with ten samples of ovarian cancer, ten samples of endometriosis, and 3 samples of eutopic endometrioid tissues as control. They were analyzed for the expression of ARID1A by RT-qPCR and ELISA, then analyzed for the activity of MnSOD as antioxidant enzyme and level of malondialdehyde as one of the oxidative stress damage effect evidence on cell's components. The second part of the study was experimental study on cultured eutopic endometrial and endometriosis cells. They were induced by H2O2 of 0, 100, and 1000 nM concentration. Analysis of the expression of ARID1A by RTqPCR and ELISA, and the DCFH-DA for the level of Reactive oxygen species were done.

Result: The impact of the H2O2 induction in repressing ARID1A gene expression on the endometriosis as well on the eutopic endometrium cells are significant, but not on the ovarian cancer in this study.

Conclusion: Oxidative stress has a role in repressing the expression of ARID1A gene at the mRNA and protein levels on the endometriosis."

"[ABSTRAKLatar Belakang: Kanker prostat adalah kanker yang paling umum pada pria. Kanker terjadi karena hilangnya kontrol atas proliferasi sel dan apoptosis sehingga sel berproliferasi terus menerus tanpa ada kematian sel. Apoptosis diregulasi oleh beberapa protein tertentu diantaranya protein keluarga Bcl-2 dan protein kanal. Perkembangan kanker prostat memerlukan transformasi dari sel epitel yang normal menjadi sel ganas yang kehilangan kemampuan untuk mengakumulasi zinc. Salah satu efek utama zinc adalah mencegah pertumbuhan sel kanker prostat dengan menginduksi apoptosis dengan memfasilitasi proses pembentukan pori Bax yang memulai apoptogenesis mitokondria. Selain keluarga Bcl-2, VDAC1 juga berperan penting dalam proses apoptosis. Beberapa penelitian menyatakan Bcl-2 mempunyai kaitan erat dengan VDAC1 terkait proses apoptosis dan protein pro-apoptotik Bax juga secara langsung berinteraksi dengan VDAC yang kemudian menginduksi keluarnya sitokrom c dari membran mitokondria.Tujuan: Mengevaluasi ekspresi mRNA dari gen mengkode keluarga protein Bcl-2 (Bax dan Bcl-2) dalam proses apoptogenesis pada galur sel kanker prostat yg diinduksi oleh zinc; Mengevaluasi ekspresi mRNA dari gen VDAC1 dalam proses apoptogenesis pada galur sel kanker prostat yang diinduksi oleh zinc; Menganalisis hubungan antara ekspresi VDAC1 dengan protein keluarga Bcl-2 pada apoptogenesis galur sel kanker prostat.Desain: Penelitian ini menggunakan eksperimental in vitro dan analisis statistikMetode: Untuk memperbanyak galur sel kanker prostat (PC3) dilakukan kultur sel, kemudian diberi perlakuan dengan tiga kelompok (kontrol, zinc 20 μM dan staurosporin 0,16 μM). Selanjutnya dilakukan isolasi RNA dan elektroforesis RNA untuk mengetahui keutuhan RNA. Terakhir dilakukan qRT PCR yang kemudian datanya dianalisis secara statistika.Hasil: Ekspresi Bax, Bcl-2 dan VDAC1 pada galur sel kanker prostat (PC-3) yang diberi perlakuan zinc mengalami penurunan dibandingkan dengan kontrol (tidak diberi perlakuan). Akan tetapi penurunan ekspresi tersebut tidak bernilai signifikan karena nilai p > 0,05 (nilai signifikansi Bax = 0,309; nilai signifikansi Bcl-2 = 0,236; nilai signifikansi VDAC1 = 0,437). VDAC1 mempunyai korelasi yang signifikan (p < 0,05) dengan Bax (p = 0,01) dibandingkan dengan Bcl-2 (p = 0,118).Kesimpulan: Terjadi perubahan ekspresi pada setiap gen (Bax, Bcl-2 dan VDAC1) pada galur sel kanker prostat yang diberi perlakuan zinc dengan yang tidak diberi perlakuan, akan tetapi tidak bernilai signifikan. VDAC1 mempunyai korelasi yang bermakna dengan Bax dan mempunyai korelasi yang tidak bermakna dengan Bcl-2.

ABSTRACT

Background: Prostate cancer is the most common cancer in men. Cancer occurs due to loss control of cell proliferation and apoptosis thus continuously proliferating cells without cell death. Apoptosis is regulated by specific proteins including Bcl-2 family proteins and channel proteins. The development of prostate cancer requires the transformation of normal epithelial cells into malignant cells that lose the ability to accumulate zinc. One of the main effects of zinc is to prevent the growth of prostate cancer cells by inducing apoptosis by facilitating the process of pore formation Bax that started apoptogenesis mitochondrial. In addition to Bcl-2 family, VDAC1 also plays an important role in the process of apoptosis. Some studies suggest Bcl-2 has close links with related VDAC1 apoptosis and pro-apoptotic protein Bax also directly interact with VDAC which then induces the release of cytochrome c from the mitochondrial membrane.

Objective: To evaluate the expression of mRNA of the gene encoding the Bcl-2 family proteins (Bax and Bcl-2) in the process apoptogenesis on prostate cancer cell line that is induced by zinc; Evaluate the mRNA expression of genes in the process VDAC1 apoptogenesis on prostate cancer cell line induced by zinc; Analyzing the relationship between the expression of VDAC1 with Bcl-2 family proteins in prostate cancer cell lines apoptogenesis.

Design: This study used an experimental in vitro and statistical analysis

Methods: To reproduce the prostate cancer cell lines (PC3) performed cell culture, then treated with three groups (control, zinc 20 μM and staurosporin 0,16 μM). Furthermore, the isolation of RNA and RNA electrophoresis to determine the integrity of the RNA. Recently performed qRT PCR and the data were analyzed statistically.

Results: The expression of Bax, Bcl-2 and VDAC1 on prostate cancer cell line (PC-3) were treated with zinc decreased than the control (untreated). However, a decrease in the expression of no significant value because the value of p > 0.05 (Bax significant value = 0.309; the value of the significance of Bcl-2 = 0.236; VDAC1 significant value = 0.437). VDAC1 has a significant correlation (p < 0.05) with Bax (p = 0.01) than Bcl-2 (p = 0.118).

Conclusion: There is a change in the expression of each gene (Bax, Bcl-2 and VDAC1) in prostate cancer cell lines that treated with zinc than untreated, but no significant value. VDAC1 has a significant correlation with Bax and had no significant correlation with Bcl-2.;Background: Prostate cancer is the most common cancer in men. Cancer occurs due to loss control of cell proliferation and apoptosis thus continuously proliferating cells without cell death. Apoptosis is regulated by specific proteins including Bcl-2 family proteins and channel proteins. The development of prostate cancer requires the transformation of normal epithelial cells into malignant cells that lose the ability to accumulate zinc. One of the main effects of zinc is to prevent the growth of prostate cancer cells by inducing apoptosis by facilitating the process of pore formation Bax that started apoptogenesis mitochondrial. In addition to Bcl-2 family, VDAC1 also plays an important role in the process of apoptosis. Some studies suggest Bcl-2 has close links with related VDAC1 apoptosis and pro-apoptotic protein Bax also directly interact with VDAC which then induces the release of cytochrome c from the mitochondrial membrane.

Objective: To evaluate the expression of mRNA of the gene encoding the Bcl-2 family proteins (Bax and Bcl-2) in the process apoptogenesis on prostate cancer cell line that is induced by zinc; Evaluate the mRNA expression of genes in the process VDAC1 apoptogenesis on prostate cancer cell line induced by zinc; Analyzing the relationship between the expression of VDAC1 with Bcl-2 family proteins in prostate cancer cell lines apoptogenesis.

Design: This study used an experimental in vitro and statistical analysis

Methods: To reproduce the prostate cancer cell lines (PC3) performed cell culture, then treated with three groups (control, zinc 20 μM and staurosporin 0,16 μM). Furthermore, the isolation of RNA and RNA electrophoresis to determine the integrity of the RNA. Recently performed qRT PCR and the data were analyzed statistically.

Results: The expression of Bax, Bcl-2 and VDAC1 on prostate cancer cell line (PC-3) were treated with zinc decreased than the control (untreated). However, a decrease in the expression of no significant value because the value of p > 0.05 (Bax significant value = 0.309; the value of the significance of Bcl-2 = 0.236; VDAC1 significant value = 0.437). VDAC1 has a significant correlation (p < 0.05) with Bax (p = 0.01) than Bcl-2 (p = 0.118).

Conclusion: There is a change in the expression of each gene (Bax, Bcl-2 and VDAC1) in prostate cancer cell lines that treated with zinc than untreated, but no significant value. VDAC1 has a significant correlation with Bax and had no significant correlation with Bcl-2., Background: Prostate cancer is the most common cancer in men. Cancer occurs due to loss control of cell proliferation and apoptosis thus continuously proliferating cells without cell death. Apoptosis is regulated by specific proteins including Bcl-2 family proteins and channel proteins. The development of prostate cancer requires the transformation of normal epithelial cells into malignant cells that lose the ability to accumulate zinc. One of the main effects of zinc is to prevent the growth of prostate cancer cells by inducing apoptosis by facilitating the process of pore formation Bax that started apoptogenesis mitochondrial. In addition to Bcl-2 family, VDAC1 also plays an important role in the process of apoptosis. Some studies suggest Bcl-2 has close links with related VDAC1 apoptosis and pro-apoptotic protein Bax also directly interact with VDAC which then induces the release of cytochrome c from the mitochondrial membrane.

Objective: To evaluate the expression of mRNA of the gene encoding the Bcl-2 family proteins (Bax and Bcl-2) in the process apoptogenesis on prostate cancer cell line that is induced by zinc; Evaluate the mRNA expression of genes in the process VDAC1 apoptogenesis on prostate cancer cell line induced by zinc; Analyzing the relationship between the expression of VDAC1 with Bcl-2 family proteins in prostate cancer cell lines apoptogenesis.

Design: This study used an experimental in vitro and statistical analysis

Methods: To reproduce the prostate cancer cell lines (PC3) performed cell culture, then treated with three groups (control, zinc 20 μM and staurosporin 0,16 μM). Furthermore, the isolation of RNA and RNA electrophoresis to determine the integrity of the RNA. Recently performed qRT PCR and the data were analyzed statistically.

Results: The expression of Bax, Bcl-2 and VDAC1 on prostate cancer cell line (PC-3) were treated with zinc decreased than the control (untreated). However, a decrease in the expression of no significant value because the value of p > 0.05 (Bax significant value = 0.309; the value of the significance of Bcl-2 = 0.236; VDAC1 significant value = 0.437). VDAC1 has a significant correlation (p < 0.05) with Bax (p = 0.01) than Bcl-2 (p = 0.118).

Conclusion: There is a change in the expression of each gene (Bax, Bcl-2 and VDAC1) in prostate cancer cell lines that treated with zinc than untreated, but no significant value. VDAC1 has a significant correlation with Bax and had no significant correlation with Bcl-2.]"

"ABSTRAKLatar Belakang: Keberadaan sel punca kanker payudara diduga berkontribusi dalam timbulnya resistensi terapi. Beberapa mekanisme yang mempengaruhi respons terapi pada kanker yaitu aktifnya jalur sinyal embrionik, hambatan apoptosis dan tingginya perbaikan DNA serta adaptasi sel punca kanker terhadap hipoksia dan stres oksidatif.Tujuan: Menganalisis profil ekspresi gen kepuncaan pada kanker payudara setelah terapi neoajuvan hormonal dan kemoterapi dilihat hubungannya dengan jalur apoptosis p53, jalur stres oksidatif NFkB dan penanda hipoksia HIF- serta respons terapi.Metode: Penelitian ini menggunakan sampel jaringan kanker payudara stadium IIIB dan IV sebelum terapi neoajuvan 46 sampel pre dan setelah terapi neoajuvan 46 sampel post . Total RNA diekstraksi kemudian dilakukan pengukuran ekspresi dengan menggunakan teknik Next Generation Sequencing Truseq targeted RNA expression Illumina dengan menggunakan panel sel punca, p53 dan NFkB. Selain itu juga ekspresi HIF-1 dan HIF-2 diukur dengan menggunakan qRT-PCR.Hasil: Setelah terapi neoajuvan, profil ekspresi gen kanker payudara yang memiliki respons molekuler yang baik pada jalur kepuncaan adalah CCNE1, CDC42, CTNNB1, HDAC2, PSEN1, PSENEN, pada jalur apoptosis adalah BIRC5, CASP8, CASP9, CDK1 dan PCNA, pada jalur stres oksidatif adalah SOD2, STAT1 dan TBK1, serta pada jalur hipoksia yaitu HIF-1 dan HIF-2 . Profil ekspresi gen dengan respons molekuler yang buruk pada jalur kepuncaan adalah ALDH1A1, ALDH2, CCND2, CXCL12, FZD7, IGF1, sedangkan pada jalur apoptosis adalah ATM dan BID. Respons histopatologis Miller Payne berkorelasi positif bermakna dengan ekspresi gen jalur apoptosis dengan respons molekuler yang baik BIRC5, CASP8, CDK1 , namun berkorelasi negatif bermakna dengan ekspresi gen ALDH1A1. Survival pasien kanker payudara berkorelasi negatif bermakna dengan ekspresi ALDH1A1 dan SOD2.Kesimpulan: Ekspresi gen ALDH1A1 dan SOD2 merupakan faktor penting untuk prediksi prognosis terapi neoajuvan sistemik pada pasien kanker payudara stadium lanjut.

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ABSTRACTIntroduction: The presence of breast cancer stem cells is considered to contribute to therapeutic resistance. There are some mechanisms affected therapy response in the cancer, such as active embryonic signaling pathways, inhibition of apoptosis and high DNA repair, adaptation to hypoxia and oxidative stress.Aim: to analyse the stemness gene expression profile in breast cancer after neoadjuvant chemotherapy and hormonal therapy correlated with apoptotic p53 , oxidative stress NFkB and hypoxia HIF- signaling pathways and also therapeutic responses.Methods: This study used breast tissue samples IIIB and IV before neoadjuvant therapy 46 pre samples and after neoadjuvant therapy 46 post samples . Total RNA was measured the expression profile using Next Generation Sequencing Truseq targeted RNA expression Illumina with stem cell, p53 and NFkB panels. In addition, HIF-1 and HIF-2 expression were measured using qRT-PCR. Results: After neoadjuvant therapy, the expression profiles of breast cancer genes that have good molecular responses in stem cells pathway are CCNE1, CDC42, CTNNB1, HDAC2, PSEN1, PSENEN, in apoptotic pathway are BIRC5, CASP8, CASP9, CDK1 and PCNA, in oxidative stress pathway are SOD2, STAT1 and TBK1, as well as in the hypoxic pathway HIF-1 and HIF-2 . Expression profiles with poor molecular responses in stem cells pathway are ALDH1A1, ALDH2, CCND2, CXCL12, FZD7, IGF1, while in apoptotic pathway are ATM and BID. Histopathologic response Miller Payne was significantly positively correlated with apoptotic pathway gene expression with good molecular response BIRC5, CASP8, CDK1 , but negatively significant correlated with ALDH1A1 gene expression. Survival of breast cancer patients significantly negatively correlated with ALDH1A1 and SOD2 expression. Conclusion: ALDH1A1 and SOD2 gene expression is an important factor for predicting the prognosis of systemic neoajuvan therapy in patients with advanced breast cancer."

"Latar Belakang : Kanker payudara merupakan salah satu penyebab kematian tertinggi akibat kanker pada wanita di Indonesia. Hal ini diantaranya disebabkan karena adanya resistensi terhadap terapi berlandaskan ROS seperti pada radioterapi maupun kemoterapi. Sel punca kanker payudara (cancer stem cells, CSCs) memiliki peran pada mekanisme resistensi ini. Penelitian terhadulu menunjukkan kemampuan CSCs untuk bertahan terhadap kondisi stress oksidatif pada pemberian rotenon. Karena itu, dalam penelitian ini dilakukan analisis terhadap faktor transkripsi NF-kB pada sel kanker payudara baik CSC maupun non CSC, terkait peran NF-kB dalam mempertahankan viabilitas sel kanker pada kondisi stress oksidatif.Metode: Penelitian dilakukan pada sel punca kanker payudara manusia (CD24-/CD44+) maupun non sel punca (CD24-/CD44-) yang diberi H2O2 dengan konsentrasi 1.1µM, 11µM, dan 110µM dengan kontrol sel yang tidak diberi H2O2. Penilaian dilakukan terhadap parameter ekspresi mRNA NF-kB, dan viabilitas sel. Uji statistik dilakukan menggunakan IBM-SPSS dengan nilai α < 0.05.Hasil: Pemberian H2O2 pada konsentrasi 11µM menunjukkan peningkatan yang signifikan pada ekspresi mRNA NFkB CSCs dibanding non CSCs (p<0.05). Sedangkan untuk hasil uji viabilitas pada seluruh konsentrasi H2O2 nampak bahwa CSCs mampu mempertahankan viabilitasnya dibandingkan dengan non CSCs yang mengalami penurunan viabilitas (p<0.05)..Kesimpulan: Kondisi stres oksidatif akibat pemberiaan H2O2 dapat meningkatkan ekspresi mRNA NF-kB pada CSCs sehingga viabilitasnya tetap dapat dipertahankan.

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Introduction: Breast cancer is one of the highest causes of death from cancer in women in Indonesia. This is partly due to the resistance to ROS-based therapies such as radiotherapy and chemotherapy. Breast cancer stem cells (cancer stem cells, CSCs) have a role in this resistance mechanism. Previous studies demonstrated the ability of CSC to survive oxidative stress conditions due to rotenone administration. Therefore, in this study an analysis was carried out on the transcription factor NF-kB in breast cancer cells, both CSCs and Non CSCs, related to the role of NF-kB in maintaining the survival of cancer cells under conditions of oxidative stress.

Methods: The study was conducted on human breast cancer stem cells (CD24-/CD44+) and non stem cells (CD24-/CD44-) which were given H2O2 at concentrations of 1.1µM, 11µM, and 110µM with control cells not given H2O2. Assessment was carried out on the parameters of NF-kB mRNA expression, and cell viability. Statistical tests were performed using IBM-SPSS with a value of α < 0.05.

Results: Administration of H2O2 at a concentration of 11µM showed a significant increase in the expression of NFk-B CSCs mRNA compared to non CSCs (p<0.05). As for the viability test results at all concentrations of H2O2 it appears that CSCs was able to maintain its viability compared to non CSCs which experienced a decrease in viability (p<0.05).

Conclusion: Conditions of oxidative stress due to administration of H2O2 can increase the expression of NF-kB mRNA in CSCs so that its viability can be maintained.

In this study, conditions of oxidative stress due to administration of H2O2 led to an increase in the expression of NF-kB mRNA in CSCs so that cell viability could be maintained."

"ABSTRAKPendahuluan: Kanker paru merupakan kanker dengan insidensi tertinggi di dunia. Tatalaksana kanker paru sampai sekarang masih menjadi tantangan. Senyawa alami antikanker mulai dikembangkan, salah satunya kedelai hitam. Kedelai hitam Glycine soja memiliki zat bioaktif yang berpotensi sebagai antikanker. Penelitian ini bertujuan untuk mengetahui kandungan metabolit sekunder dan tingkat toksisitas ekstrak etanol kedelai hitam terhadap sel kanker paru A549. Metode: Identifikasi kandungan ekstrak etanol kedelai hitam dilakukan dengan uji kromatografi lapis tipis KLT dan uji fitokimia. Uji sitotoksisitas dilakukan dengan MTT-assay secara in vitro. Variasi konsentrasi yang digunakan pada penelitian ini adalah 6,25, 12,5, 25, 50, 100, 200, 400, dan 800 ug/ml. Hasil dan Pembahasan: Hasil uji KLT menunjukkan bahwa terdapat 6 senyawa pada ekstrak etanol kedelai hitam. Hasil uji fitokimia membuktikan bahwa kedelai hitam mengandung flavonoid, alkaloid, saponin, tanin, triterpenoid, dan glikosida yang memiliki potensi sebagai antikanker. Ekstrak etanol kedelai hitam menunjukkan aktivitas sitotoksik yang moderat pada sel kanker paru A549 IC50= 114,51 ug/ml , sedikit dibawah cisplatin IC50= 85,45 ug/ml sebagai kontrol positif. Konsentrasi ekstrak tertinggi 800 ug/ml memberikan persentase inhibisi tertinggi 83,8 dan nilai optical density yang berbeda bermakna dengan konsentrasi lainnya

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ABSTRACTIntroduction Lung cancer incidence is the highest incidence of cancer in the world. Management of lung cancer is still a challenge today. The natural anticancer compounds are being developed, one of which is black soybeans. Black soybean Glycine soja has bioactive compounds that has potential as anticancer. Objective of this research is to determine the secondary metabolite content and toxicity level of black soybean ethanol extract to A549 lung cancer cell. Method Identification of the content of black soybean ethanol extract was performed by thin layer chromatography TLC and phytochemical test. The cytotoxicity test performed was in vitro MTT assay. The concentration variations used in this study were 6,25, 12,5, 25, 50, 100, 200, 400, and 800 ug ml. Results and Discussion The TLC results show that there were 6 compounds in black soybean ethanol extract. Phytochemical test results prove that Glycine soja contains flavonoids, alkaloids, saponins, tannins, triterpenoids, and glycosides that have potential as anticancer. Black soybean ethanol extract show moderate cytotoxic activity in A549 cells IC50 114,51 ug ml , slightly below cisplatin IC50 85,45 ug ml as a positive control. The highest extract concentration 800 ug ml give highest percentage inhibition 83,8 and significantly different optical density with other concentrations p"

"ABSTRAKJengkol (Archidendron pauciflorum) merupakan tanaman yang tumbuh di AsiaTenggara, dan biji jengkol telah menjadi makanan khas di berbagai negara tersebut.Biji jengkol dipercaya memiliki sejumlah manfaat antioksidan karena adanyakandungan asam jengkol, vitamin C, polifenol dan flavonoid. Asam jengkolmerupakan senyawa dengan gugus sulfur yang dipercaya memiliki sifat antioksidan.Tujuan penelitian ini adalah menentukan efek antioksidan dari ekstrak biji jengkolterhadap stres oksidatif sel yang disebabkan oleh radikal bebas. Hidrogen peroksidadigunakan untuk menginduksi stres oksidatif pada sel darah merah domba secara invitro, diikuti dengan pengikuran aktivitas spesifik katalase. Penelitian laboratoriumeksperimental ini dilakukan pada lima perlakuan yang berbeda, di mana ekstrak bijijengkol diberikan sebelum dan sesudah induksi stres oksidatif oleh hidrogenperoxide. Hasil penelitian menunjukkan penurunan yang signifikan dalam aktivitasspesifik katalase dalam sel darah merah dengan penamahan ekstrak biji jengkol, baikdi kelompok kuratif dan preventif. Dengan demikian, penambahan ekstrak bijijengkol menurunkan aktivitas spesifik katalase, kemungkinan dikarenakan olehpembentukan senyawa II katalase. Inaktivasi enzim katalase dapat mencegahpenguraian hidrogen peroksida sebagai senyawa radikal bebas.

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ABSTRACTJengkol is a plant that grows natively in Southeast Asia, and its seeds has become atypical food in these various countries. Jengkol beans are believed to carry antioxidantproperties due to its contents of djencolic acid, vitamin C, polyphenols andflavonoids. Djencolic acid is an organosulfur compound and is thought to haveantioxidant benefits. In this study, we aim to determine the antioxidant effects ofjengkol bean extract against cellular oxidative stress induced by free radicals.Hydrogen peroxide is used to induce oxidative stress in sheep red blood cells in vitro,followed by measurement of catalase specific activity. This laboratory experimentalstudy was conducted on five different treatments, where jengkol bean extract isadministered both before and after induction of oxidative stress by hydrogenperoxide. Results showed a significant decrease in catalase specific activity in redblood cells with added jengkol bean extract, both in the curative and preventivegroups. Thus, the addition of jengkol bean extract decreases catalase specific activityin red blood cells, possibly through formation of compound II. The inactivation ofcatalase may prevent eradication of hydrogen peroxide as a free radical."

"Terapi fotodinamik yang dimediasi asam aminolevulinat (ALA-PDT) merupakan salah satu terapi kanker yang efektif dan minim efek samping. Terapi ini menggunakan ALA untuk mendorong akumulasi selektif protoporfirin IX (PpIX) yang dapat memicu pembentukan spesi oksigen reaktif toksik di dalam sel kanker. Namun, efektivitas ALA-PDT dapat dihambat oleh kerja transporter ABCG2 dan ABCB1 yang menghalangi akumulasi PpIX. Hemin berpotensi menjadi zat kombinasi untuk meningkatkan efektivitas ALA-PDT karena memiliki sifat antitumor dan dapat memengaruhi ekspresi DKK1 sebagai inhibitor jalur Wnt/β-catenin, jalur yang berkaitan dengan regulasi ABCG2 dan ABCB1. Penelitian ini menganalisis pengaruh pemberian kombinasi hemin dan ALA setelah 48 jam pada sel kanker paru-paru A549 terhadap viabilitas sel, akumulasi PpIX intraseluler, ekspresi gen DKK1, ABCG2, ABCB1, serta ekspresi protein ABCG2 dan ABCB1 menggunakan metode uji MTT, HPLC, RT-qPCR, dan western blotting. Hasil menunjukkan bahwa pemberian kombinasi hemin dan ALA yang diikuti fotoiradiasi menurunkan viabilitas sel A549. Akumulasi PpIX intraseluler meningkat setelah perlakuan. Ekspresi gen DKK1 mengalami penurunan, menunjukkan bahwa penurunan viabilitas dan peningkatan akumulasi PpIX tidak melalui penghambatan jalur Wnt/β-catenin oleh DKK1. Ekspresi ABCG2, baik mRNA maupun protein, menurun setelah perlakuan, sedangkan ekspresi ABCB1 meningkat. Hasil tersebut dapat menunjukkan bahwa ABCG2 lebih berperan dibandingkan dengan ABCB1 dalam akumulasi PpIX pada sel A549.

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Aminolevulinic acid-mediated photodynamic therapy (ALA-PDT) is an effective cancer treatment with minimal side effects. ALA-PDT utilizes ALA to induce selective accumulation of protoporphyrin IX that can trigger the formation of toxic reactive oxygen species within cancer cells. However, ALA-PDT effectiveness can be hindered by ABCG2 and ABCB1 transporters impeding PpIX accumulation. Hemin is a potential substance to combine with ALA due to its antitumor properties and influence on the DKK1 gene expression as a Wnt/β-catenin inhibitor, regulating ABCG2 and ABCB1. This study analyzed the effects of a combination of hemin and ALA after 48 hours on A549 lung cancer cells regarding cell viability, intracellular PpIX accumulation, DKK1, ABCG2, ABCB1 gene expression, and ABCG2 and ABCB1 protein expression, using MTT assay, HPLC, RT-qPCR, and western blotting. The results indicate that the combination of hemin and ALA followed by photoirradiation decreased the viability of A549 cells. Intracellular PpIX accumulation increased after treatment. The DKK1 gene expression decreased, indicating that the decrease in viability and the increase in PpIX accumulation did not occur through the inhibition of the Wnt/β-catenin pathway by DKK1. The expression of ABCG2, both mRNA and protein, decreased after treatment, while ABCB1 expression increased. This result suggests that ABCG2 plays a greater role than ABCB1 in PpIX accumulation in A549 cancer cells."