Premium
miR‐511 inhibits proliferation and metastasis of breast cancer cells by targeting FGF4
Author(s) -
Zhang Chao,
Yang Ting,
Jiang Hongchuan
Publication year - 2020
Publication title -
the journal of gene medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.689
H-Index - 91
eISSN - 1521-2254
pISSN - 1099-498X
DOI - 10.1002/jgm.3168
Subject(s) - breast cancer , metastasis , cancer research , cell growth , cancer , biology , ca 15 3 , medicine , pathology , oncology , ca15 3 , genetics
Background The present study aimed to explore the functions and molecular mechanisms of miR‐511 in breast cancer. Methods A quantitative real‐time polymerase chain reaction (qRT‐PCR) was used to detect miR‐511 levels in breast cancer tissues; a chi‐squared test was used to analyze the relationship between miR‐511 expression level and pathological parameters of breast cancer patients; the proliferation of breast cancer cell lines MDA‐MB‐231 and MCF‐7 was determined by the cell counting kit‐8 (CCK‐8) assay; migration was determined by scratch wound healing assay and transwell assay; TargetScan was used to predict the binding site between the 3'‐untranslated region (3'‐UTR) of fibroblast growth factor 4 (FGF4) and miR‐511; and qRT‐PCR, western blot and a luciferase reporter gene assay were conducted to further validate the targeting relationship between miR‐511 and FGF4. Results The expression level of miR‐511 was lower in breast cancer tissues than that in adjacent normal tissues. Low expression of miR‐511 was associated with larger tumor size, lymph node metastasis and short survival time. In vitro experiments showed that miR‐511 modulated the proliferation and metastasis of breast cancer cells. It was also confirmed that miR‐511 directly targeted 3'‐UTR of FGF4 and reduced its expression, and FGF4 overexpression reversed the effect of miR‐511 on the malignant phenotypes of breast cancer cells. Conclusions The results obtained in the present study demonstrate that miR‐511 inhibits breast cancer proliferation and metastasis by down‐regulating FGF4 expression, which may be helpful in the development of new treatment strategies for breast cancer.