miR‑125a‑5p and miR‑7 inhibits the proliferation, migration and invasion of vascular smooth muscle cell by targeting EGFR.

Abstract:

:The ectopic proliferation, migration and invasion of vascular smooth muscle cells (VSMCs) contributes to the progression of various human vascular diseases. Accumulating evidence has demonstrated that microRNAs (miRs) exert vital functions in the proliferation and invasion of VSMCs. The current study aimed to elucidate the functions of miR‑125a‑5p and miR‑7 in VSMCs and investigate the associated molecular mechanisms. The results of EdU and reverse transcription‑quantitative PCR assays revealed that platelet‑derived growth factor (PDGF)‑BB enhanced the proliferation of VSMCs and significantly reduced the expression of miR‑125a‑5p and miR‑7. miR‑125a‑5p or miR‑7 overexpression significantly ameliorated PDGF‑BB‑induced proliferation, migration and invasion of VSMCs. Furthermore, the results demonstrated that epidermal growth factor receptor (EGFR) may be a target mRNA of miR‑125a‑5p and miR‑7 in VSMCs. The results of western blot analysis indicated that co‑transfection of miR‑125a‑5p mimics or miR‑7 mimics distinctly decreased the protein expression of EGFR in EGFR‑overexpressed VSMCs. Moreover, rescue experiments indicated that EGFR overexpression alleviated the suppressive impact of the miR‑125a‑5p and miR‑7 s on the growth, migration and invasion of VSMCs. In conclusion, the current study identified that miR‑125a‑5p and miR‑7 repressed the growth, migration and invasion of PDGF‑BB‑stimulated VSMCs by, at least partially, targeting EGFR. The current study verified that miR‑125a‑5p and miR‑7 may be used as feasible therapeutic targets for cardiovascular diseases.

journal_name

Mol Med Rep

authors

Zhou H,Lin S,Hu Y,Guo D,Wang Y,Li X

doi

10.3892/mmr.2021.12347

keywords:

["epidermal growth factor receptor","growth","invasion vascular smooth muscle cells","micro RNA‑125a‑5p","micro RNA‑7","migration"]

subject

Has Abstract

pub_date

2021-10-01 00:00:00

issue

4

eissn

1791-2997

issn

1791-3004

pii

708

journal_volume

24

pub_type

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