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

Y.-K. Ma, T.-H. Shen, X.-Y. Yang

Intervention Department of Shanghai Xuhui District Central Hospital, Shanghai, China. qiang355luyunwud@163.com

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• Oncology

OBJECTIVE: The long non-coding RNA, FAM83H antisense RNA 1 (head to head) (FAM83H-AS1), has been reported to function as an oncogene in some types of cancer. However, the role of lncRNA FAM83H-AS1 in hepatocellular carcinoma (HCC) still remains unknown. The present work aims to explore the effect of lncRNA FAM83H-AS1 on cell proliferation and cell invasion in HCC.
PATIENTS AND METHODS: 66 pairs of HCC tissue samples and adjacent normal tissues were collected, and the expression level of lncRNA FAM83H-AS1 was detected by quantitative Reverse Transcription-Polymerase Chain Reaction (qRT-PCR) analysis. Cell Counting Kit-8 (CCK-8) assay was performed to detect cell proliferation ability, and transwell assays were applied to observe the effect of lncRNA FAM83H-AS1 on cell migration and invasion. QRT-PCR and Western blot analysis was used to determine the mRNA and protein expression.
RESULTS: In the present study, our results confirmed that lncRNA FAM83H-AS1 expression was overexpressed in HCC tissues relative to the adjacent normal tissues. Furthermore, higher lncRNA FAM83H-AS1 expression significantly associated with tumor size and vascular invasion in patients with HCC. The Kaplan-Meier methods and log rank test demonstrated that increased lncRNA FAM83H-AS1 expression associated with shorter patient overall survival compared to lower lncRNA FAM83H-AS1 expression in patients with HCC. Moreover, function assays by CCK-8 cell proliferation and transwell cell migration and invasion assays showed that the knockdown of lncRNA FAM83H-AS1 significantly inhibited cell proliferation, migration, and invasion ability in HCC. Moreover, we found that the downregulating expression of lncRNA FAM83H-AS1 inhibited Wnt/β-catenin pathway by reducing β-catenin and WNT1 expression in HCC cells.
CONCLUSIONS: Together, our results indicated that it plays an important role in HCC progression and may be a potential target for HCC treatment.

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