Journal
JOURNAL OF PHARMACY AND PHARMACOLOGY
Volume 73, Issue 9, Pages 1212-1217Publisher
OXFORD UNIV PRESS
DOI: 10.1093/jpp/rgab042
Keywords
ovarian cancer; ANRIL; proliferation; apoptosis; Wnt/beta-catenin
Categories
Ask authors/readers for more resources
The study demonstrated that down-regulation of lncRNA ANRIL effectively suppressed OVCAR-3 cell proliferation and invasion, induced apoptosis, and prevented Wnt/β-catenin signal transduction.
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/beta-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/beta-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/beta-catenin signal transduction.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available