MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3

MiR-548 has been reported to be involved in a variety of tumor processes, but its function in breast cancer remains unclear. In this study, we found that miR-548 was low expressed in breast cancer tissues and cells compared with normal control. We then examined whether up-regulation of miR-548 could...

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Published in:Cytotechnology (Dordrecht) 2020-10, Vol.72 (5), p.751-761
Main Authors: Tan, Pei-Yi, Wen, Liu-Jing, Li, Hua-Nan, Chai, Shi-Wei
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recordid cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7547945
title MiR-548c-3p inhibits the proliferation, migration and invasion of human breast cancer cell by targeting E2F3
format Article
creator Tan, Pei-Yi
Wen, Liu-Jing
Li, Hua-Nan
Chai, Shi-Wei
subjects Antibodies
Apoptosis
Biochemistry
Biomedicine
Biotechnology
Breast cancer
Cancer therapies
Cell migration
Cell proliferation
Cells
Chemistry
Chemistry and Materials Science
Chinese medicine
MicroRNAs
Original
Original Article
Up-regulation
ispartof Cytotechnology (Dordrecht), 2020-10, Vol.72 (5), p.751-761
description MiR-548 has been reported to be involved in a variety of tumor processes, but its function in breast cancer remains unclear. In this study, we found that miR-548 was low expressed in breast cancer tissues and cells compared with normal control. We then examined whether up-regulation of miR-548 could improve the progression of breast cancer. Our results indicate that up-regulation of miR-548 significantly inhibits cell proliferation, migration andinvasion, and induces apoptosis in breast cancer cells. Further studies showed that miR-548 could specifically inhibit E2F3 expression. Moreover, rescue test showed that up-regulation of E2F2 could reverse the effect of miR-548 on proliferation, migration, invasion and apoptosis of breast cancer cells. In general, miR-548 could improve the progression of breast cancer. By targeting E2F2, which may make a potential target for the treatment of breast cancer.
language eng
source SpringerLink Contemporary; PubMed
identifier ISSN: 0920-9069
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1573-0778
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