Effect of miR-196a inhibition on esophageal cancer growth in vitro.

Published on Feb 1, 2020in Anti-Cancer Drugs2.26
· DOI :10.1097/CAD.0000000000000823
Minghua Bai1
Estimated H-index: 1
(Xi'an Jiaotong University),
Yiping Dong6
Estimated H-index: 6
(Xi'an Jiaotong University)
+ 3 AuthorsSuxia Han18
Estimated H-index: 18
(Xi'an Jiaotong University)
Esophageal cancer has recent shown a higher incidence but lower 5-year survival rate after normal clinical treatment in China. The aim of this study was to observe whether the inhibition of miR-196a affects esophageal cancer cell growth by modulating the nuclear factor-kappaB target gene and to detect the possible cooperative therapeutic effects on esophageal cancer by knocking down miR-196a expression combined with the specific inhibitor of nuclear factor-kappaB target genes. Thus, anti-miR-196a or sotrastaurin, a protein kinase C (PKC) inhibitor, were used to alter PKC expression. We found that miR-196a knockdown or PKC inhibition by sotrastaurin changed PKC expression which then reduced esophageal cancer cell proliferation and downregulated proliferating cell nuclear antigen expression via the classical B-cell receptor-PKC nuclear factor-kappaB pathway but not the alternative pathway; in addition, miR-196a inhibition can increase the caspase level and induce esophageal cancer cell apoptosis. Our current results provided the evidence that miR-196a was related to the classical nuclear factor-kappaB pathway, and these new findings proved the potential therapeutic effect of miR-196a in targeted therapy for clinical esophageal cancer patients.
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