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논문 기본 정보

자료유형
학술저널
저자정보
Xiyao Yin (College of Food and Drugs, Luoyang Polytechnic, Luoyang, China) Xin Liu (Department of Central Laboratory, The 989th Hospital, Luoyang, China) Hui Gong (Department of Central Laboratory, The 989th Hospital, Luoyang, China) Zhiliang Chu (College of Food and Drugs, Luoyang Polytechnic, Luoyang, China)
저널정보
대한부인종양학회 Journal of Gynecologic Oncology Journal of Gynecologic Oncology Vol.35 No.4
발행연도
2024.7
수록면
1 - 16 (16page)
DOI
https://doi.org/10.3802/jgo.2024.35.e97

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Objective: Cer vical cancer (CC) is a serious gynecologic health issue for women worldwide. Long non-coding RNA (lncRNA) has been well-documented in controlling malignantbehavior of various cancer cells. The role of lncRNA STARD7-AS1 in regulating CC cellproliferation and autophagy and its possible mechanism were investigated in this work. Methods: RNA expression and protein levels were quantified by reverse transcriptionquantitative polymerase chain reaction and western blotting. The location of STARD7-AS1in CC cells was examined using subcellular fraction assays. Cell Counting Kit-8 assaysand colony forming assays were performed to measure CC cell viability and proliferation. Autophagy in CC cells was evaluated using macrophage-derived chemokine (MDC) stainingand transmission electron microscopy. The binding between microRNA (miR)-31-5p andSTARD7-AS1 (or thioredoxin-interacting protein [TXNIP]) was determined by performingluciferase reporter, RNA pull-down or RNA immunoprecipitation assays. Results: STARD7-AS1 overexpression significantly suppressed CC cell viability andproliferation while notably inducing autophagy. STARD7-AS1 upregulated TXNIPexpression via interaction with miR-31-5p. In addition, the effects of STARD7-AS1 on CC cellproliferation and autophagy were reversed by TXNIP silencing. The suppressive effect ofSTARD7-AS1 overexpression on phosphor ylated levels of mTOR and S6K1 was counter vailedby TXNIP deficiency. Conclusion: In conclusion, lncRNA STARD7-AS1 inhibits CC cell proliferation and promotescell autophagy by targeting the miR-31-5p/TXNIP axis to inactivate the mTOR signaling.

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