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Long non-coding RNA XIST regulates miR-106b-5p/P21 axis to suppress tumor progression in renal cell carcinoma
Ke Sun1, Zhankui Jia2, Ranran Duan3
1Department of Urology, The First Affiliated Hospital, Zhengzhou University, No 1 Jianshe East Rd., Zhengzhou, 450052, People's Republic of China; Urological Institute of Henan, Zhengzhou, 450052, Henan Province, People's Republic of China.
Abstract:
Long non-coding RNAs (lncRNAs) have been demonstrated to exert important roles in cancer development and progression. The biological function of lncRNA X-inactive specific transcript (XIST) in the development of renal cell carcinoma (RCC) and the underlying mechanisms are still largely unknown. In this study, we found that XIST was down-regulated in RCC tissues and cells. Overexpression of XIST significantly suppressed cell proliferation and induced cell G0/G1 arrest in vitro and inhibited tumor growth in vivo. We further found that XIST could directly interact with miR-106b-5p and increase the expression of P21. Thus, XIST positively regulated the expression of P21 through sponging miR-106b-5p, and played a tumor suppressor role in RCC. Moreover, we found that curcumin could regulate XIST/miR-106b-5p/P21 axis in RCC cells. Our study exhibits the role of XIST as a miRNA sponge in RCC and supports the potential application of XIST in RCC therapy.
Insights
Long non-coding RNA XIST is downregulated in renal cell carcinoma (RCC). Upregulating XIST inhibits RCC progression by regulating the miR-106b-5p/P21 axis, suggesting therapeutic potential.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Long non-coding RNAs (lncRNAs) are critical in cancer.
- The role of lncRNA XIST in renal cell carcinoma (RCC) is unclear.
Purpose of the Study:
- Investigate XIST's function and mechanism in RCC.
- Explore XIST's potential as a therapeutic target.
Main Methods:
- Quantitative real-time PCR to assess XIST expression.
- In vitro and in vivo assays to evaluate XIST's functional impact.
- MiRNA interaction analysis (e.g., luciferase assay) to elucidate mechanisms.
Main Results:
- XIST expression is reduced in RCC tissues and cells.
- XIST overexpression suppresses RCC cell proliferation and induces G0/G1 arrest.
- XIST directly targets miR-106b-5p, upregulating P21 expression.
- Curcumin affects the XIST/miR-106b-5p/P21 pathway in RCC cells.
Conclusions:
- XIST acts as a tumor suppressor in RCC by sponging miR-106b-5p and regulating P21.
- The XIST/miR-106b-5p/P21 axis presents a novel therapeutic strategy for RCC.
- XIST holds promise for RCC treatment and warrants further investigation.
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