期刊
MOLECULAR CANCER
卷 13, 期 -, 页码 -出版社
BIOMED CENTRAL LTD
DOI: 10.1186/1476-4598-13-261
关键词
HCC; miR-610; Proliferation; Wnt/beta-catenin; LRP6; TBL1X
资金
- National Natural Science Foundation of China [81000959, 81201781]
- Guangdong Natural Science Foundation [S2013010016023, 10451130001004472]
- Science and Technology Planning Project of Guangdong Province, China [2009B030801007]
- Science and Technology Program of Guangzhou Municipal Government [2013 J4100081]
- Foundation of Science and Technology Innovation of Zengcheng [ZC201004]
- Fundamental Research Funds for the Central Universities [12ykpy47, 12ykpy43]
- National 12th Five-Year Science and Technology Plan Major Projects of China [2012ZX10002017 -005]
- Guangzhou Municipal Health Bureau [20141A011117]
Background: Wnt/beta-catenin signaling pathway plays important roles in human cancer progression. Better understanding the mechanism underlying regulation of Wnt/beta-catenin signaling pathway might provide novel therapeutic targets for cancer treatment. Methods: miR-610 expression levels in hepatocellular carcinoma (HCC) cell lines, HCC tissues and 76 archived HCC specimens were determined using real-time PCR. Cell viability was measured by 3-[4, 5-dimethylthiazol-2-yl]-2, 5-diphenyltetrazolium bromide (MTT) assay. The level of DNA synthesis was determined by BrdU incorporation assay. Flow cytometry analysis was used to analyze cell cycle progression. The cells proliferation and tumorigenesis were determined by colony formation and anchorage-independent growth assays in vitro, and by xenograft tumors in vivo. Luciferase assay and micro-ribonucleoprotein complex immunoprecipitation assay were used to confirm the association of the targeted mRNAs with miR-610. Results: miR-610 was downregulated in human HCC cells and tissues, and correlated with HCC progression and patient survival. Inhibition of miR-610 promoted, but overexpression of miR-610 reduced, HCC cell proliferation and tumorigenicity both in vitro and in vivo. Furthermore, we found that inhibiting miR-610 activated, but overexpressing miR-610 decreased, the Wnt/beta-catenin activity through directly suppressing lipoprotein receptor-related protein 6 (LRP6) and transducin beta-like protein 1 (TBL1X). The in vitro analysis was consistent with the inverse correlation detected between miR-610 levels with expression of LRP6 and TBL1X in a cohort of human HCC samples. Conclusions: Our results indicate that miR-610 downregulation plays essential roles in HCC progression and reduced miR-610 is correlated with Wnt/beta-catenin signaling pathway.
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