MicroRNA192 inhibits cell proliferation and induces apoptosis in human breast cancer by targeting caveolin 1.
Oncol Rep
; 42(5): 1667-1676, 2019 Nov.
Article
in En
| MEDLINE
| ID: mdl-31485620
It has been demonstrated that microRNA192 (miR192) serves important roles in different cancer types, including breast cancer, prostate cancer and colorectal cancer. However, its biological role and function in breast cancer remains largely unknown. The present study aimed to determine the role of miR192 in breast cancer. In the present study, one normal breast and two breast tumor cells lines were used, which included the normal mammary fibroblast cell line Hs578Bst, a more aggressive breast tumor cell line MDAMB231 and a less aggressive breast tumor cell line MCF7. The effect of miR192 on proliferation of breast cancer cells was detected with an MTT assay. Western blot analysis was performed to determine protein expression of caveolin 1 (CAV1). A lentiviral vector that overexpresses premiR192 and control lentiviral packaging plasmids were used in the present study. The Student's ttest was performed to analyze the significance of differences between samples. In the present study, it was determined that the expression of miR192 is downregulated in breast cancer, compared with the adjacent normal tissues. Overexpression of miR192 significantly inhibited cell proliferation, and induced cell apoptosis and cell cycle arrest in MCF7 and MDAMB231 cells. Using a bioinformatics method, CAV1 was considered a potential target of miR192. Furthermore, it was demonstrated that CAV1 is a direct target of miR192 and its protein expression is negatively regulated by miR192. Therefore, the present study demonstrated that miR192 serves an important role as a regulator in breast cancer and the miR192/CAV1 axis has a potential as a therapeutic target for treatment of breast cancer.
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Breast Neoplasms
/
MicroRNAs
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Caveolin 1
Limits:
Aged
/
Animals
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Female
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Humans
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Middle aged
Language:
En
Journal:
Oncol Rep
Journal subject:
NEOPLASIAS
Year:
2019
Document type:
Article
Country of publication: