Down-regulation of microRNA-10a mediates the anti-tumor effect of icaritin in A549 cells via the PTEN/AKT and ERK pathway.

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.

journal_name

Gen Physiol Biophys

authors

Lu X,Xue B,Zhang T,Zhou X,Zhang Y

doi

10.4149/gpb_2019041

subject

Has Abstract

pub_date

2019-11-01 00:00:00

pages

525-533

issue

6

eissn

0231-5882

issn

1338-4325

journal_volume

38

pub_type

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