Long noncoding RNAs (lncRNAs) play vital roles in the development and progression of hepatocellular carcinoma (HCC). The recent study finds a strong correlation between lncRNA small nucleolar RNA host gene 7 (SNHG7) and HCC metastasis. However, the molecular mechanism by which SNHG7 regulates HCC progression has not been investigated. In this study, we found that SNHG7 was highly expressed in HCC tissues compared to non-tumor tissues. Data from public databases consistently indicated the up-regulated expression of SNHG7 in HCC. Furthermore, the levels of SNHG7 were up-regulated in four HCC cell lines (Huh7, Hep3B, HCCLM3, MHCC97 H) compared with LO2 cells. Interestingly, the elevated expression of SNHG7 was closely correlated with advanced tumor stages, high tumor grades, vascular invasion and poor prognosis of HCC. Knockdown of SNHG7 markedly inhibited cell proliferation, migration and invasion in HCCLM3 and MHCC97H cells, and prominently suppressed the growth and metastasis of HCCLM3 cells in vivo. Mechanistically, SNHG7 silencing increased the level of miR-122-5p in HCC cells. Luciferase reporter assay revealed the direct interaction between SNHG7 and miR-122-5p. Moreover, SNHG7 knockdown decreased the levels of ribosomal protein L4 (RPL4) mRNA and protein in HCC cells. Accordingly, the stability of RPL4 mRNA was reduced by SNHG7 silencing. More importantly, either miR-122-5p knockdown or RPL4 restoration partially reversed SNHG7 silencing-induced tumor suppressive effects on HCC cells. In conclusion, we demonstrated that SNHG7 expression was up-regulated in HCC. SNHG7 contributed to HCC progression by regulating miR-122-5p and RPL4. Therefore, SNHG7 might be a potential biomarker and therapeutic target for HCC.
Keywords: Hepatocellular carcinoma; RPL4; SNHG7; Tumor progression; miR-122-5p.
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