LncRNA CRNDE promotes hepatocellular carcinoma cell proliferation, invasion, and migration through regulating miR‐203/ BCAT1 axis
Journal of Cellular Physiology
Published online on September 19, 2018
Abstract
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- "\nAbstract\n\nObjective\nTo investigate the impact of long noncodingRNA (lncRNA)
colorectal neoplasia differentially expressed (CRNDE) on hepatocellular cancer (HCC)
cell propagation, invasion, and migration by mediating miR‐203/\nBCAT1 axis.\n\n\nMethods\nMicroarray
analysis was based on 25 pairs of HCC cancerous tissues and adjacent tissues. The
expression levels of CRNDE, miR‐203, and BCAT1 in HCC tissues were analyzed by quantitative
real‐time polymerase chain reaction (qRT‐PCR). The liver cell line L‐02 and HCC
cell lines HepG2 and Huh‐7 were utilized to assess the regulatory effects of CRNDE
and miR‐203 on HCC progression in vitro. Western blot was used to qualify BCAT1
protein expression level. Cell proliferation and apoptosis were evaluated using
CCK‐8 and flow cytometry analysis, whereas cell invasion and migration assay were
performed by the Transwell assay. The relationship among CRNDE, miR‐203, and \nBCAT1
was validated by dual luciferase assay. Tumor Xenograft study was established to
verify the pathological effect of CRNDE on HCC development in vivo.\n\n\nResults\nThe
expression levels of the CRNDE and BCAT1 were upregulated in HCC tissues and cells,
whereas miR‐203 was downregulated in HCC. Knockdown of CRNDE or miR‐203 overexpression
would inhibit HCC cell propagation and metastasis, and induced cell apoptosis. Moreover,
miR‐203 was negatively correlated with CRNDE, the same as miR‐203 with \nBCAT1.
Dual luciferase assay showed that miR‐203 was an inhibitory target of CRNDE, and
\nBCAT1 was directly targeted by miR‐203 as well.\n\n\nConclusion\nLncRNA CRNDE
could enhance HCC tumorgenesis by sponging miR‐203 and mediating BCAT1. LncRNA CRNDE
might facilitate HCC cell propagation, invasiveness, and migration through regulating
miR‐203/\nBCAT1 axis.\n"
- Journal of Cellular Physiology, EarlyView.