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ABSTRAKPendahuluan: 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
ABSTRAKIntroduction: 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., 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.]
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