Long non-coding RNA HCG11 sponging miR-522-3p inhibits the tumorigenesis of non-small cell lung cancer by upregulating SOCS5.
Long non-coding RNA HCG11 sponging miR-522-3p inhibits the tumorigenesis of non-small cell lung cancer by upregulating SOCS5.
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DOI:
10.1111/1759-7714.13624
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发表时间:
2020-10
期刊:
影响因子:
2.9
通讯作者:
Chu F
中科院分区:
文献类型:
--
作者:
Fan G;Jiao J;Shen F;Ren Q;Wang Q;Chu F
Numerous studies have shown that long non‐coding RNA (lncRNA) is involved in various human diseases including non‐small cell lung cancer (NSCLC). The aim of this study was to explore the potential role of lncRNA HCG11 in the pathogenesis of NSCLC. The mRNA expression of HCG11, miR‐522‐3p and SOCS5 was detected by RT‐qPCR. The regulatory mechanism of lncRNA HCG11 was investigated by CCK‐8, transwell and dual luciferase reporter assays. Downregulation of lncRNA HCG11 and upregulation of miR‐522‐3p were found in NSCLC tissues and cells, and abnormal expressions of lncRNA HCG11 and miR‐522‐3p were related to adverse clinical outcomes of NSCLC patients. LncRNA HCG11 acted as a molecular sponge for miR‐522‐3p. Functionally, lncRNA HCG11 inhibited cell viability, migration and invasion in NSCLC by downregulating miR‐522‐3p. Further, miR‐522‐3p directly targeted SOCS5. lncRNA HCG11 could positively regulate SOCS5 expression in NSCLC. In addition, HCG11 downregulation or miR‐522‐3p overexpression abolished the inhibitory effect of SOCS5 on cell viability, migration and invasion in NSCLC. LncRNA HCG11 inhibits cell viability, migration and invasion in NSCLC by functioning as a ceRNA of miR‐522‐3p to upregulate SOCS5. Downregulation of lncRNA HCG11 is related to adverse clinical outcomes in NSCLC patients. HCG11 has been shown to inhibit cell viability and motility in NSCLC, and HCG11 functions as a ceRNA of miR‐522‐3p to upregulate SOCS5.
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