Long non-coding RNA 657 suppresses hepatocellular carcinoma cell growth by acting as a molecular sponge of miR-106a-5p to regulate PTEN expression

• Published in: The international journal of biochemistry & cell biology 2017-11, Vol.92, p.34-42
• Main Authors: Hu, Bingren, Cai, Huajie, Zheng, Ru, Yang, Shouzhang, Zhou, Zhenxu, Tu, Jinfu
• Format: Article
• Language: English
• Subjects: Animals; Carcinoma, Hepatocellular - genetics; Carcinoma, Hepatocellular - pathology; Cell Cycle - genetics; Cell Line, Tumor; Cell Movement - genetics; Cell Proliferation - genetics; Cell Transformation, Neoplastic; Female; Gene Expression Regulation, Neoplastic - genetics; Gene Knockdown Techniques; Hepatocellular carcinoma; Humans; LINC00657; Liver Neoplasms - genetics; Liver Neoplasms - pathology; Long non-coding RNA; Male; Mice; MicroRNAs - genetics; Middle Aged; miR-106a-5p; Neoplasm Invasiveness; PTEN; PTEN Phosphohydrolase - genetics; RNA, Long Noncoding - genetics
• ISSN: 1357-2725; 1878-5875
• DOI: 10.1016/j.biocel.2017.09.008

•LINC00657 is down-regulated in HCC tissues and malignant HCC cell lines and associated with good outcomes.•LINC00657 inhibits cell proliferation, cell cycle, migration and invasion.•LINC00657 is a direct target of miR-106a-5p.•LINC00657 improves PTEN expression by down-regulating the miR-106a-5p level. Previous study has identified the aberrant expression of LINC00657, a long non-coding RNA (lncRNA), in human breast cancer. However, the expression pattern, biological function and underlying mechanism of LINC00657 in human hepatocellular carcinoma (HCC) remain obscure. The expression levels of LINC00657 in HCC tissues and cell lines were determined by quantitative real-time PCR. CCK-8 assay, cell colony formation assay, cell cycle analysis, Transwell assay were performed to determine whether LINC00657 could affect HCC progression. Luciferase reporter assay was used to assess the target of LINC00657. Expressions of the relevant proteins were analyzed by Western blot. Herein, we found that LINC00657 was downregulated in HCC tissue specimens as well as in malignant HCC cell lines. LINC00657 overexpression inhibited the proliferation, migration and invasion of HCC cells, while LINC00657 depletion promoted both cell viability and cell invasion in vitro. We also found that LINC00657 could inhibit tumor growth in vivo. Further experiments demonstrated that down-regulated LINC00657 increased the expression of miR-106a-5p. miR-106a-5p decreased the abundances of PTEN protein, while had no impact on PTEN mRNA. Moreover, we identified that both LINC00657 and PTEN mRNA were targets of miR-106a-5p by using dual-luciferase reporter assay. Our results provide the new evidence supporting the tumor-suppressive role of LINC00657 in HCC, suggesting that LINC00657 might play a role in HCC and can be a novel therapeutic target for treating HCC.