MiR-181c affects estrogen-dependent endometrial carcinoma cell growth by targeting PTEN
Lili Zhuang1, Hongmei Qu2, Jianxiang Cong1
1Department of Center for Reproductive Medicine, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, China.
Abstract:
MicroRNAs (miRNAs), which is a type of non-coding and single-stranded small molecule RNA, bind either completely or incompletely to 3'-UTR of the target gene mRNA to inhibit mRNA translation or degradation. In our study, we aimed to explore the roles and mechanisms of miR-181c in the apoptosis of RL95-2 human endometrial carcinoma cells. Cell activity and apoptosis were detected by cell counting Kit-8 (CCK-8) assay and flow cytometry (FCM), respectively. Related mRNAs and proteins expression was determined by quantitative real-time reverse transcription PCR (qRT-PCR) and western blot assays, respectively. The binding capacity of PTEN-3'-UTR and miR-181c was assessed by luciferase reporter assay. The obtained results suggested that E2 evidently increased the cell activity of RL95-2 cells. In addition, miR-181c inhibitor suppressed the cell viability and enhanced the apoptosis capacity of E2-induced RL95-2 cells and distinctly reduced the miR-181c expression. We also found that miR-181c could bind to PTEN-3'-UTR and miR-181c inhibitor up-regulated the expression level of PTEN in E2-induced RL95-2 cells. Besides, overexpression of PTEN markedly promoted the apoptosis of E2-induced RL95-2 cells through regulating the Bax and Bcl-2 expression, and modulated the expression of AKT pathway, p53 and Cyclin D. In conclusion, our findings revealed that miR-181c affected the estrogen-dependent endometrial carcinoma cell growth by targeting PTEN. The potential effects of miR-181c on the apoptosis of E2-induced RL95-2 cells suggest that miR-181c could be an effective target for endometrial carcinoma therapies.
Insights
MicroRNAs (miRNAs) regulate endometrial cancer cell growth. miR-181c targets PTEN, promoting apoptosis in estrogen-dependent cancer cells, suggesting it as a potential therapeutic target.
Area of Science:
- Molecular Biology
- Genetics
- Oncology
Background:
- MicroRNAs (miRNAs) are small non-coding RNAs regulating gene expression by binding to mRNA targets.
- Endometrial carcinoma is an estrogen-dependent cancer with complex regulatory mechanisms.
- Understanding miRNA roles is crucial for developing targeted cancer therapies.
Purpose of the Study:
- To investigate the role and mechanism of miR-181c in the apoptosis of RL95-2 human endometrial carcinoma cells.
- To determine if miR-181c affects estrogen-induced cell activity and apoptosis.
- To identify the molecular targets of miR-181c in this cellular context.
Main Methods:
- Cell viability assessed using cell counting Kit-8 (CCK-8) assay.
- Apoptosis detected by flow cytometry (FCM).
- Gene and protein expression analyzed via qRT-PCR and Western blot; miRNA-target interaction confirmed by luciferase reporter assay.
Main Results:
- Estrogen (E2) increased RL95-2 cell activity.
- miR-181c inhibition suppressed cell viability and enhanced apoptosis in E2-treated cells.
- miR-181c directly targets PTEN, upregulating its expression and promoting apoptosis via Bax/Bcl-2, AKT, p53, and Cyclin D modulation.
Conclusions:
- miR-181c influences estrogen-dependent endometrial carcinoma cell growth by targeting PTEN.
- miR-181c promotes apoptosis in E2-induced RL95-2 cells.
- miR-181c represents a potential therapeutic target for endometrial carcinoma treatment.
Related Concept Videos
Frequency-dependent Selection
Cells Coordinate Growth and Proliferation
Contact-dependent Signaling
Gap Junctions
In animal cells, gap junctions are formed...
Population Growth
Drug Dependence
Meristems and Plant Growth


