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- Title
Long noncoding RNA ZFPM2-AS1 regulates ITGB1 by miR-1226-3p to promote cell proliferation and invasion in hepatocellular carcinoma.
- Authors
LIU, W.; ZHANG, G.-Q.; ZHU, D.-Y.; WANG, L.-J.; LI, G.-T.; XU, J.-G.; JIN, X.-L.; ZHU, Y.-M.; YANG, X.-Y.
- Abstract
OBJECTIVE: Long noncoding RNA (lncRNA) is emerging as a vital regulator in various tumors. However, the biological function of ZFPM2-antisense RNA 1 (ZFPM2-AS1) in hepatocellular carcinoma (HCC) remains unclear. The present study aims to explore the function and mechanism of ZFPM2-AS1 in hepatocellular carcinoma progression. PATIENTS AND METHODS: The ZFPM2-AS1 expression in HCC cells and tissues was measured by quantitative real-time polymerase chain reaction (qRT-PCR). Effects of ZFPM2-AS1 on tumor cell proliferation and invasion were detected by CCK8 assay or EdU assay or matrigel migration assay and Western blot. The Luciferase reporter assay, RNA pulldown assay, qRT-PCR, and Western blot were performed to explore and confirm the interaction between ZFPM2-AS1 and miR-1226-3p and integrin β1 (ITGB1). RESULTS: ZFPM2-AS1 was overexpressed in HCC tissues and cell lines. High levels of ZFPM2- AS1 were correlated with advanced TNM stage, distant metastasis and a poorer overall survival rate. ZFPM2-AS1 knockdown inhibited cell proliferation and invasion. ZFPM2-AS1 could directly bind to and negatively regulate miR-1226-3p expression. Moreover, ITGB1 was identified as a target gene of miR-1226-3p. ITGB1 was found to be directly negatively regulated by miR-1226-3p and indirectly upregulated by ZFPM2-AS1. Rescue assays demonstrated that ZFPM2-AS1 promotes HCC cell proliferation and invasion through modulating miR-1226/ITGB1 axis. CONCLUSIONS: ZFPM2-AS1 promotes cell proliferation and migration by regulating miR- 1226-3p/ITGB1 axis in HCC.
- Subjects
NON-coding RNA; HEPATOCELLULAR carcinoma; CELL proliferation; POLYMERASE chain reaction; CELL migration
- Publication
European Review for Medical & Pharmacological Sciences, 2020, Vol 24, Issue 14, p7612
- ISSN
1128-3602
- Publication type
Article