[ABSTRAK Pendahuluan: Endometriosis merupakan suatu kelainan jinak ginekologi yangdapat mengalami transformasi menjadi kanker. Stres oksidatif diduga berperandalam perkembangan penyakit endometriosis. Gen supresor tumor ARID1Abanyak ditemukan termutasi dan inaktif pada kanker ovarium yang berhubungandengan endometriosis. Tujuan penelitian adalah untuk menganalisis peran stresoksidatif terhadap ekspresi gen supresor tumor ARID1A dalam transformasiendometriosis menjadi ganas.Metoda: Penelitian dimulai dengan 10 sampel jaringan kanker ovarium, 10 sampelendometriosis dan3 jaringan endometrium eutopik sebagai kontrol yang diisolasimRNA dan proteinnya. Analisis ekspresi gen ARID1A pada tingkat mRNAdilakukan dengan pemeriksaan RT-qPCR dan pada tingkat protein dengan ELISA.Pada sel endometriosis dan kanker ovarium dilakukan analisis stres oksidatif denganpemeriksaan aktivitas antioksidan MnSOD dan pemeriksaan kadar MDA sebagaisalah bukti kerusakan salah satu komponen sel. Setelah itu dilakukan ujieksperimental pada kultur sel endometriosis dan endometrium eutopik sebagaikontrol. Kedua sel kultur diinduksi dengan H2O2 konsentrasi 0 nM, 100 nM, dan1000 nM. Analisis dilakukan terhadap ketahanan hidup sel, kadar ROS dan ekspresigen ARID1A pada tingkat mRNA dan protein.Hasil: Efek induksi H2O2 dalam menekan ekspresi gen ARID1A sel endometriosisdan 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 supresortumor ARID1A ditingkat mRNA dan protein pada endometriosis ABSTRAK Introduction: Endometriosis as a gynecologic benign lesion, can transform itselfinto cancer. Oxidative stress is considered as an important factor in endometriosisdevelopment. Studies found that ARID1A as tumor suppressor gene, wasfrequently mutated and inactivated in endometriosis associated ovarian cancer.The aim of the study is to analyze the role of oxidative stress on ARID1Aexpresion in endometriosis malignant transformation.Methods: This study started with ten samples of ovarian cancer, ten samples ofendometriosis, and 3 samples of eutopic endometrioid tissues as control. Theywere analyzed for the expression of ARID1A by RT-qPCR and ELISA, thenanalyzed for the activity of MnSOD as antioxidant enzyme and level ofmalondialdehyde as one of the oxidative stress damage effect evidence on cell’scomponents. The second part of the study was experimental study on culturedeutopic endometrial and endometriosis cells. They were induced by H2O2 of 0,100, and 1000 nM concentration. Analysis of the expression of ARID1A by RTqPCRand ELISA, and the DCFH-DA for the level of Reactive oxygen specieswere done.Result: The impact of the H2O2 induction in repressing ARID1A gene expressionon the endometriosis as well on the eutopic endometrium cells are significant, butnot on the ovarian cancer in this study.Conclusion: Oxidative stress has a role in repressing the expression of ARID1Agene at the mRNA and protein levels on the endometriosis., Introduction: Endometriosis as a gynecologic benign lesion, can transform itselfinto cancer. Oxidative stress is considered as an important factor in endometriosisdevelopment. Studies found that ARID1A as tumor suppressor gene, wasfrequently mutated and inactivated in endometriosis associated ovarian cancer.The aim of the study is to analyze the role of oxidative stress on ARID1Aexpresion in endometriosis malignant transformation.Methods: This study started with ten samples of ovarian cancer, ten samples ofendometriosis, and 3 samples of eutopic endometrioid tissues as control. Theywere analyzed for the expression of ARID1A by RT-qPCR and ELISA, thenanalyzed for the activity of MnSOD as antioxidant enzyme and level ofmalondialdehyde as one of the oxidative stress damage effect evidence on cell’scomponents. The second part of the study was experimental study on culturedeutopic endometrial and endometriosis cells. They were induced by H2O2 of 0,100, and 1000 nM concentration. Analysis of the expression of ARID1A by RTqPCRand ELISA, and the DCFH-DA for the level of Reactive oxygen specieswere done.Result: The impact of the H2O2 induction in repressing ARID1A gene expressionon the endometriosis as well on the eutopic endometrium cells are significant, butnot on the ovarian cancer in this study.Conclusion: Oxidative stress has a role in repressing the expression of ARID1Agene at the mRNA and protein levels on the endometriosis.] |