LncRNA SNHG15 promotes hepatocellular carcinoma progression by sponging miR-141-3p.

Small nucleolar RNA host gene 15 (SNHG15) is a long noncoding RNA (lncRNA), which promotes progression of multiple cancers. Its specific function in hepatocellular carcinoma (HCC), however, is uncertain. The aims of our study were, therefore, to explore the role of SNHG15 in HCC. SNHG15 and miR-141-3p expression were assessed via quantitative real-time PCR (qRT-PCR) in 58 paired HCC samples and adjacent matched adjacent normal tissues. CCK-8 assay, flow cytometric examination, and wound healing/invasion assays were used to respectively assess how SNHG15 influences cell proliferation, the cell cycle, and the migratory and invasive potential of HCC cells. MicroRNA (miRNAs) that targeted SNHG15 was screened by Starbase2.0 and identified by RNA immunoprecipitation and luciferase reporter assays. SNHG15 expression was markedly increased, whereas miR-141-3p expression was substantially reduced in HCC cells and tissue samples relative to normal controls. When SNHG15 was knocked down, this resulted in a significant disruption to the proliferation, as well as the invasive and migratory ability of these HCC cells. miR-141-3p was also found to be an SNHG15 target in HCC cells. Furthermore, miR-141-3p inhibitor partially reversed the observed SNHG15 depletion-mediated reduction in HCC proliferation, migration, and invasion. By repressing miR-141-3p, SNHG15 could modulate zinc finger E-box binding homeobox 2 (ZEB2) and E2F transcription factor 3 (E2F3) expression, both of which are miR-141-3p targets. These finding suggested that SNHG15 promoted HCC progression via negative regulation of miR-141-3p, thus identifying a potential novel HCC treatment pathway.

Ye J ，Tan L ，Fu Y ，Xu H ，Wen L ，Deng Y ，Liu K ... -  《-》

lncRNA-SNHG15 accelerates the development of hepatocellular carcinoma by targeting miR-490-3p/ histone deacetylase 2 axis.

Hepatocellular carcinoma (HCC) has become a great threat for people's health. Many long noncoding RNAs are involved in the pathogenesis of HCC. SNHG15, as a tissue specific long noncoding RNAs, has been studied in many human cancers, except HCC. To explore the regulatory mechanism of SNHG15 in HCC. In the present research, 101 HCC patient samples, two HCC cell lines and one normal liver cell line were used. RT-qPCR and Western blot analysis were applied to detect SNHG15, miR-490-3p and histone deacetylase 2 (HDAC2) expression. The regulatory mechanism of SNHG15 was investigated using CCK-8, Transwell and luciferase reporter assays. Our research showed that up-regulation of SNHG15 was found in HCC and was related to aggressive behaviors in HCC patients. Moreover, knockdown of SNHG15 restrained HCC cell proliferation, migration and invasion. In addition, SNHG15 served as a molecular sponge for miR-490-3p. Further, miR-490-3p directly targets HDAC2. HDAC2 was involved in HCC progression by interacting with the SNHG15/miR-490-3p axis. In conclusion, long noncoding RNA SNHG15 promotes HCC progression by mediating the miR-490-3p/HDAC2 axis in HCC.

Dai W ，Dai JL ，Tang MH ，Ye MS ，Fang S ... -  《-》

Long noncoding RNA matrilineal expression gene 3 inhibits hepatocellular carcinoma progression by targeting microRNA-5195-3p and regulating the expression of forkhead box O1.

Li M ，Liao H ，Wu J ，Chen B ，Pang R ，Huang J ，Zhu Y ... -  《-》

LncRNA SNHG1 promotes cell progression and metastasis via sponging miR-377-3p in hepatocellular carcinoma.

Qu A ，Yang Q 《NEOPLASMA》

LncRNA TMPO-AS1 promotes hepatocellular carcinoma cell proliferation, migration and invasion through sponging miR-329-3p to stimulate FOXK1-mediated AKT/mTOR signaling pathway.

Hepatocellular carcinoma (HCC) is one of the leading causes of cancer-related death worldwide. Numerous analyses have revealed the abnormal expression of long non-coding RNAs (lncRNAs) in HCC cells. This study aims to explore biological functions of lncRNA TMPO-AS1 (TMPO antisense RNA 1) in HCC cell proliferation, apoptosis, invasion and migration. The gene expression in HCC tissues and cell lines were measured by qRT-PCR. The role of TMPO-AS1 in HCC was confirmed by CCK-8, colony formation, TUNEL, transwell and western blot as well as by in vivo experiments. RNA pull down and luciferase reporter assays were utilized to prove the binding relationship between TMPO-AS1/FOXK1 (forkhead box K1) andmiR-329-3p. Rescue assays elucidated the regulatory effects of TMPO-AS1/miR-329-3p/FOXK1/AKT/mTOR pathway on cellular activities in HCC. TMPO-AS1was upregulated in HCC tissues and cells and its depletion inhibits HCC cell proliferation, invasion, migration, and EMT process as well as tumor growth. Furthermore, TMPO-AS1 could bind with miR-329-3p, which suppressed HCC cell proliferation. FOXK1 served as the target gene of miR-329-3p and TMPO-AS1 upregulated FOXK1 by sponging miR-329-3p in HCC cells. Additionally, FOXK1 overexpression or miR-329-3p inhibitor neutralized the repressing effects of TMPO-AS1 knockdown on HCC development. Finally, it verified that TMPO-AS1 could regulate AKT/mTOR pathway via FOXK1 to promote HCC. TMPO-AS1 contributes to HCC progression by sponging miR-329-3p to activate FOXK1-mediated AKT/mTOR signaling pathway.

Guo X ，Wang Y 《Cancer Medicine》