Upregulation of miR-650 is correlated with down-regulation of ING4 and progression of hepatocellular carcinoma

Background In the last decade, studies in hepatocellular carcinoma (HCC) demonstrate dysregulation of miRNAs expression. For instance, miR‐650 has been implicated in gastric and colorectal cancer tumorigenicity; however, the role of miR‐650 remains unknown in HCC. Methods In this study, we performed...

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Veröffentlicht in:Journal of surgical oncology 2013-02, Vol.107 (2), p.105-110
Hauptverfasser: Zeng, Zhao-lin, Li, Fu-jun, Gao, Feng, Sun, Dong-sheng, Yao, Lei
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Sprache:eng
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Zusammenfassung:Background In the last decade, studies in hepatocellular carcinoma (HCC) demonstrate dysregulation of miRNAs expression. For instance, miR‐650 has been implicated in gastric and colorectal cancer tumorigenicity; however, the role of miR‐650 remains unknown in HCC. Methods In this study, we performed a comprehensive analysis to examine the miR‐650 expression level in 248 HCC and 120 paracarcinomatous liver (PCL) tissues. The correlations between miR‐650 expression level and the clinicopathological characteristics (HCC tumorigenicity) were evaluated. The role of miR‐650 played in HCC was investigated by Q‐PCR, western blot, and MTT. Results We found that miR‐650 expression was significantly increased in HCC patients and significantly associated with the patients' age (P = 0.0019), differentiation capability (P = 0.0108), and also tumor stage (P = 0.0069). Moreover, we compared the expression level of both ING4 and miR‐650 in 122 HCC patients by western blot and real‐time PCR. Statistical result showed a significant negative correlation between them (rs = −0.2011, P = 0.0264). Transfection and MTT test suggested that miR‐650 decreased the expression of ING4 and stimulate liver cells proliferation significantly. Conclusion These data suggested that miR‐650 is correlated with the pathogenesis of HCC and is involved in the HCC tumorigenesis process by inhibiting the expression of ING4. J. Surg. Oncol. 2013;107:105–110. © 2012 Wiley Periodicals, Inc.
ISSN:0022-4790
1096-9098
DOI:10.1002/jso.23210