Let-7c Inhibits NSCLC Cell Proliferation by Targeting HOXA1

Zhan, Min; Qu, Qiang; Wang, Guo; Liu, Ying-Zi; Tan, Sheng-Lan; Lou, Xiao-Ya; Yu, Jing; Zhou, Hong-Hao

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자료유형: 학술저널

저자정보: Zhan, Min (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University) Qu, Qiang (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University) Wang, Guo (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University) Liu, Ying-Zi (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University) Tan, Sheng-Lan (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University) Lou, Xiao-Ya (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University) Yu, Jing (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University) Zhou, Hong-Hao (Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South University)

저널정보: 아시아태평양암예방학회 Asian Pacific journal of cancer prevention : APJCP Asian Pacific journal of cancer prevention : APJCP 제14권 제1호

발행연도: 2013.1

수록면: 387 - 392 (6page)

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Objective: The aim of the present study was to explore mechanisms by which let-7c suppresses NSCLC cell proliferation. Methods: The expression level of let-7c was quantified by qRT-PCR. A549 and H1299 cells were transfected with let-7c mimics to restore the expression of let-7c. The effects of let-7c were then assessed by cell proliferation, colony formation and cell cycle assay. Mouse experiments were used to confirm the effect of let-7c on tumorigenicity in vivo. Luciferase reporter assays and Western blotting were performed to identify target genes for let-7c. Results: HOXA1 was identified as a novel target of let-7c. MTS, colony formation and flow cytometry assays demonstrated that forced expression of let-7c inhibited NSCLC cell proliferation by inducing G1 arrest in vitro, consistent with inhibitory effects induced by knockdown of HOXA1. Mouse experiments demonstrated that let-7c expression suppressed tumorigenesis. Furthermore, we found that let-7c could regulate the expression of HOXA1 downstream effectors CCND1, CDC25A and CDK2. Conclusions: Collectively, these results demonstrate let-7c inhibits NSCLC cell proliferation and tumorigenesis by partial direct targeting of the HOXA1 pathway, which suggests that restoration of let-7c expression may thus offer a potential therapeutic intervention strategy for NSCLC.

#Let-7c #NSCLC #HOXA1 #G1 arrest

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Zhan, Min

소속기관 Institute of Clinical Pharmacology, Hunan Key Laboratory of Pharmacogenetics, Central South Universi