دورية أكاديمية

Down-regulation of long non-coding RNA antisense non-coding RNA in the INK4 locus suppresses OVCAR-3 cells proliferation and induction of apoptosis by Wnt/ß-catenin.

التفاصيل البيبلوغرافية
العنوان: Down-regulation of long non-coding RNA antisense non-coding RNA in the INK4 locus suppresses OVCAR-3 cells proliferation and induction of apoptosis by Wnt/ß-catenin.
المؤلفون: Lingna Sun, Yuping Cui, Kongdi Jiang, Juan Li
المصدر: Journal of Pharmacy & Pharmacology; Sep2021, Vol. 73 Issue 9, p1212-1217, 6p
مصطلحات موضوعية: LINCRNA, ANTISENSE RNA, NON-coding RNA, INHIBITION of cellular proliferation, CELL proliferation, CATENINS, CELL death
مستخلص: Objectives Ovarian cancer is a lethal gynecological malignancy. Long non-coding RNA antisense non-coding RNA in the INK4 locus (lncRNA ANRIL) was reported to have a critical role in cancer advancement. The ANRIL-mediated oncogenic underlying molecular mechanisms are not fully understood in ovarian cancer. We aimed to study ANRIL silencing effects on the proliferation and apoptosis of OVCAR-3 cells. Methods The ANRIL was Knockdown by transfection of OVCAR-3 cells with si-RNA against ANRIL. MTT assay and cell death ELISA kit were used to evaluate cellular proliferation and apoptosis. The expression levels of ANRIL, pro-and anti-apoptotic genes were assessed using q-RT-PCR. Western blotting was used to assess Wnt/ß-catenin signalling pathway. Key findings ANRIL down-regulating in OVCAR-3 cell lines resulted in significant inhibition of cellular proliferation, apoptosis induction, as well as suppression of cellular invasion. Besides, knockdown of ANRIL led to pro-apoptotic genes up-regulation, Bad and Bax and anti-apoptotic genes down-regulation, Bid and Bcl-2. More importantly, we observed that ANRIL inhibition suppressed the vital components expression of the Wnt/ß-catenin cascade. Conclusion Our findings showed that down-regulation of lncRNA ANRIL resulted in the effective suppression of OVCAR-3 cell proliferation and invasion and induction of apoptosis by preventing Wnt/ß-catenin signal transduction. [ABSTRACT FROM AUTHOR]
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قاعدة البيانات: Complementary Index