FAM83H-AS1/miR-485-5p/MEF2D axis facilitates proliferation, migration and invasion of hepatocellular carcinoma cells.

Abundant evidence has manifested that long noncoding RNAs (lncRNAs) are closely implicated in human cancers, including hepatocellular carcinoma (HCC). Remarkably, lncRNA FAM83H antisense RNA 1 (FAM83H-AS1) has been reported to be a tumor-propeller in multiple cancers. However, its effect on HCC progression remains unknown. FAM83H-AS1 expression was analyzed by RT-qPCR. Colony formation, EdU, and flow cytometry as well as transwell assays were implemented to analyze the biological functions of FAM83H-AS1 on HCC progression. Luciferase reporter, RIP and RNA pull-down assays were implemented to detect the interaction among FAM83H-AS1, microRNA-485-5p (miR-485-5p), and myocyte enhancer factor 2D (MEF2D) in HCC cells. FAM83H-AS1 expression in HCC cells was markedly elevated. FAM83H-AS1 accelerated cell proliferation, migration and invasion whereas inhibiting cell apoptosis in HCC. Besides, we confirmed that FAM83H-AS1 acts as a miR-485-5p sponge in HCC cells. Additionally, MEF2D was verified to be a direct target of miR-485-5p. FAM83H-AS1 could upregulate MEF2D expression via sponging miR-485-5p. Further, rescue experiments testified that MEF2D upregulation or miR-485-5p downregulation offset the repressive effect of FAM83H-AS1 depletion on HCC cell progression. FAM83H-AS1 facilitates HCC malignant progression via targeting miR-485-5p/MEF2D axis, suggesting that FAM83H-AS1 may be a promising biomarker for HCC treatment in the future.

Zhao W ，Guo J ，Li H ，Cai L ，Duan Y ，Hou X ，Diao Z ，Shao X ，Du H ，Li C ... -  《BMC CANCER》

Long non-coding RNA AGAP2-AS1, functioning as a competitive endogenous RNA, upregulates ANXA11 expression by sponging miR-16-5p and promotes proliferation and metastasis in hepatocellular carcinoma.

Liu Z ，Wang Y ，Wang L ，Yao B ，Sun L ，Liu R ，Chen T ，Niu Y ，Tu K ，Liu Q ... -  《JOURNAL OF EXPERIMENTAL & CLINICAL CANCER RESEARCH》

ZSCAN16-AS1 expedites hepatocellular carcinoma progression via modulating the miR-181c-5p/SPAG9 axis to activate the JNK pathway.

Liu J ，Liu R ，Liu Y ，Li L ，Cao H ，Liu J ，Cao G ... -  《-》

Upregulation of LncRNA FAM83H-AS1 in hepatocellular carcinoma promotes cell proliferation, migration and invasion by Wnt/β-catenin pathway.

Ma YK ，Shen TH ，Yang XY 《-》

RNF185-AS1 promotes hepatocellular carcinoma progression through targeting miR-221-5p/integrin β5 axis.

Recently, long noncoding RNAs (lncRNAs) have been reported to play important role in the pathogenesis of various cancers. However, the functions of RNF185-AS1 in hepatocellular carcinoma (HCC) remain unknown. The RNF185-AS1 expression in HCC cells and tissues was measured by quantitative real-time polymerase chain reaction (qRT-PCR). The effects of RNF185-AS1 on tumor cell proliferation, migration and invasion were assessed by Cell Counting Kit-8 (CCK8) assay, colony formation assay, transwell assay. The luciferase reporter assay, RNA-binding protein immunoprecipitation assay, qRT-PCR and Western blot were performed to explore and confirm the interaction between RNF185-AS1 and miR-221-5p and integrin β5. The role of RNF185-AS1 in tumor progression was explored through in vivo experiments. RNF185-AS1 was highly expressed in HCC tissues and cell lines. High levels of RNF185-AS1 were correlated with advanced TNM stage, distant metastasis and a poorer overall survival rate. RNF185-AS1 knockdown inhibited cell proliferation, migration and invasion. Additionally, RNF185-AS1 acted as a sponge for miR-221-5p and integrin β5 was identified as a target gene of miR-221-5p. Rescue assays showed that miR-221-5p inhibitor or integrin β5 overexpression rescued the function of RNF185-AS1 knockdown on cell proliferation, migration, and invasion. Moreover, we found that RNF185-AS1 knockdown inhibited tumor growth and metastasis. Our study demonstrates that RNF185-AS1 is a new oncogenic lncRNA in HCC and suggests that the RNF185-AS1/miR-221-5p/integrin β5 axis might be a potential therapeutic target for HCC.

Huang C ，Li K ，Huang R ，Zhu J ，Yang J ... -  《-》