Home FOR AUTHORS General Physiology and Biophysics 2019 General Physiology and Biophysics Vol.38, No.6, p.525–533, 2019

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Quarterly, 80 pp. per issue
Founded: 1982
ISSN  1338-4325 (online)

Published in English

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General Physiology and Biophysics Vol.38, No.6, p.525–533, 2019

Title: Down-regulation of microRNA-10a mediates the anti-tumor effect of icaritin in A549 cells via the PTEN/AKT and ERK pathway
Author: Xiangdong Lu, Beiyun Xue, Tingrong Zhang, Xie Zhou, Yao Zhang

Abstract: Icaritin, a prenylflavonoid derivative from Epimedium Genus, has been reported to exhibit tumor inhibitory effects on many types of tumor cells. Numerous studies have demonstrated that microRNAs (miRs) involve in the biological process of carcinogenesis by controlling expression of their target mRNAs to facilitate tumor growth, invasion, angiogenesis, and immune evasion. miR-124 was reported to involve in the icaritin-induced mitochondrial apoptosis in human carcinoma cells. However, the roles of other miRs in the anti-tumor effects of icaritin and its underlying mechanisms still need to be elucidated. In the present study, realtime-PCR results showed that miR-10a was significantly down-regulated after icaritin treatment in human non-small cell lung cancer cells (A549). Over-expression of miR-10a in A549 cells dramatically abrogated the anti-tumor effects of icaritin on cell proliferation, apoptosis, migration, while suppression of miR-10a partially reproduced the anti-tumor effects of icaritin. Furthermore, we found that the regulation of miR-10a in the anti-tumor effects of icaritin was mediated via the PTEN/AKT/ERK pathway by directly targeting to PTEN. Taken together, miR-10a targets PTEN to mediate the anti-tumor effect of icaritin in A549 cells, which provides a novel insight into the anti-tumor mechanism of icaritin and may provide a new strategy for lung cancer therapy.

Keywords: Icaritin, miR-10a, PTEN, A549 cells, Lung cancer
Published online: 27-Nov-2019
Year: 2019, Volume: 38, Issue: 6 Page From: 525, Page To: 533

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