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http://purl.uniprot.org/citations/23534758http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/23534758http://www.w3.org/2000/01/rdf-schema#comment"

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."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.org/dc/terms/identifier"doi:10.7314/apjcp.2013.14.1.387"xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Qu Q."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Wang G."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Tan S.L."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Yu J."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Zhan M."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Liu Y.Z."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Zhou H.H."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/author"Lou X.Y."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/date"2013"xsd:gYear
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/name"Asian Pac J Cancer Prev"xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/pages"387-392"xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/title"Let-7c inhibits NSCLC cell proliferation by targeting HOXA1."xsd:string
http://purl.uniprot.org/citations/23534758http://purl.uniprot.org/core/volume"14"xsd:string
http://purl.uniprot.org/citations/23534758http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/23534758
http://purl.uniprot.org/citations/23534758http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/23534758
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http://purl.uniprot.org/uniprot/#_P58876-mappedCitation-23534758http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/23534758
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