DANCR contributed to hepatocellular carcinoma malignancy via sponging miR-216a-5p and modulating KLF12.

Long noncoding RNA (lncRNA) differentiation antagonizing nonprotein coding RNA (DANCR) has been identified as an oncogene in several cancers. However, the biological function and role of DANCR in hepatocellular carcinoma (HCC) remain unclear. Our current study aimed to investigate the detailed mechanism of DANCR in HCC. We found that DANCR was significantly upregulated in HCC cell lines in comparison to LO2 cells. Then, we observed that knockdown of DANCR could greatly inhibit Huh7 and HepG2 cell proliferation. In addition, HCC cell apoptosis was increased by silence of DANCR and meanwhile, cell cycle progression was blocked in G1 phase. Apart from these, downregulation of DANCR repressed HCC cell migration and invasion ability obviously. As predicted by the bioinformatics analysis, microRNA-216a-5p (miR-216a-5p) could serve as a direct target of DANCR. MiR-216a-5p has been reported to be involved in many cancers. Here, the correlation between miR-216a-5p and DANCR was confirmed using dual-luciferase reporter assay and radioimmunoprecipitation assay. Subsequently, Kruppel-like factor 12 (KLF12) exerts an important role in different tumor types. KLF12 can function as a downstream target of miR-216a-5p. Finally, the in vivo experiments were used and the data proved that DANCR also strongly suppressed HCC tumor growth in vivo via targeting miR-216a-5p and KLF12. In conclusion, our study indicated that DANCR might provide a new perspective for HCC treatment.

Wang J ，Pu J ，Zhang Y ，Yao T ，Luo Z ，Li W ，Xu G ，Liu J ，Wei W ，Deng Y ... -  《-》

LncRNA DANCR regulates the growth and metastasis of oral squamous cell carcinoma cells via altering miR-216a-5p expression.

Qu XH ，Shi YL ，Ma Y ，Bao WW ，Yang L ，Li JC ，Zhang F ... -  《Human Cell》

LncRNA SNHG7 accelerates the proliferation, migration and invasion of hepatocellular carcinoma cells via regulating miR-122-5p and RPL4.

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.

Yang X ，Sun L ，Wang L ，Yao B ，Mo H ，Yang W ... -  《-》

LINC00460 promotes hepatocellular carcinoma development through sponging miR-485-5p to up-regulate PAK1.

LncRNAs can function as significant regulators of tumor development. However, their roles in hepatocellular carcinoma (HCC) remain poorly investigated. LINC00460 has been identified in several cancers, which can act as an oncogene. In this study, we observed that LINC00460 was significantly up-regulated in HCC cells, which implied that LINC00460 was involved in HCC development. Then, LINC00460 was silenced in Hep3B and Huh-7 cells and we found that knockdown of LINC00460 greatly inhibited HCC cell proliferation. In addition, HCC cell apoptosis was induced and meanwhile, cell cycle progression was blocked by down-regulation of LINC00460 in vitro. Furthermore, we proved that Hep3B and Huh-7 cell migration and invasion capacity was repressed by decrease of LINC00460. Recently, a growing number of studies have indicated the correlation between lncRNAs and microRNAs. Currently, we displayed that miR-485-5p was greatly decreased in HCC cells and LINC00460 could sponge miR-485-5p to regulate HCC progression. The binding association between LINC00460 and miR-485-5p was confirmed using dual-luciferase reporter assay, RNA pulled down and RIP assay in our research. Subsequently, PAK1 was predicted as a downstream target of miR-485-5p and we demonstrated that miR-485-5p suppressed PAK1 levels in vitro. Finally, in vivo experiments were conducted to validate that knockdown of LINC00460 repressed HCC development through modulating miR-485-5p to increase PAK1. Taken these together, we indicated that LINC00460 promoted HCC progression through sponging miR-485-5p and up-regulating PAK1.

Tu J ，Zhao Z ，Xu M ，Chen M ，Weng Q ，Ji J ... -  《-》

Crosstalk between lncRNA DANCR and miR-125b-5p in HCC cell progression.

Yang L ，Jiang MN ，Liu Y ，Wu CQ ，Liu H ... -  《-》