MiR-646 prevents proliferation and progression of human breast cancer cell lines by suppressing HDAC2 expression.
Apoptosis
Breast Neoplasms
/ genetics
Case-Control Studies
Cell Line, Tumor
Cell Proliferation
Cell Survival
Disease Progression
Down-Regulation
Epigenesis, Genetic
Female
Gene Expression Regulation, Neoplastic
HEK293 Cells
Histone Deacetylase 2
/ genetics
Humans
MCF-7 Cells
MicroRNAs
/ genetics
Up-Regulation
Breast cancer
Cancer progression
HDAC2
miR-646
Journal
Molecular and cellular probes
ISSN: 1096-1194
Titre abrégé: Mol Cell Probes
Pays: England
ID NLM: 8709751
Informations de publication
Date de publication:
10 2020
10 2020
Historique:
received:
29
04
2020
revised:
20
07
2020
accepted:
05
08
2020
pubmed:
11
8
2020
medline:
14
7
2021
entrez:
11
8
2020
Statut:
ppublish
Résumé
Breast cancer is a type of cancer with a high incidence and mortality rate worldwide. Change in epigenetic mechanisms enhances cancer cell progression. Histon deacetylase 2 (HDAC2) was found to act as a potential oncogene in different malignancies. For better understanding the mechanisms related to breast cancer development, we investigated the role of HDAC2 in breast cancer and the inhibitory effect of miR-646 on this oncogene. A total of thirty cancerous tissues and 30 adjacent non-cancerous specimens and also three breast cancer cell lines were enrolled in the study. Quantitative reverse transcriptase PCR (qRT-PCR) was employed to detect the HDAC2 and miR-646 expression level in the studied samples. The biological roles of HDAC2 and miR-646 were investigated through manipulating the expression level of HDAC2 or miR-646 in breast cancer cells. Finally, we evaluated whether the HDAC2 is a direct target for miR-646. In this study, we found HDAC2 is significantly upregulated in cancerous specimens and cell lines compared to non-cancerous tissues and normal cell line. On the other hand, miR-646 expression was decreased in clinical specimens and breast cancer cells compared to non-cancerous samples. Knocking out of the HDAC2 and overexpression of miR-646 inhibited breast cancer cell growth but promoted cell death, while untreated groups showed inverse results. Furthermore, we showed that in the breast cancer cells, miR-646 regulates the progression and proliferation by suppressing HDAC2. Taken together, our study identified a miR-646/HDAC2 regulatory function in the breast cancer development and introduced a therapeutically target for breast cancer.
Sections du résumé
BACKGROUND
Breast cancer is a type of cancer with a high incidence and mortality rate worldwide. Change in epigenetic mechanisms enhances cancer cell progression. Histon deacetylase 2 (HDAC2) was found to act as a potential oncogene in different malignancies. For better understanding the mechanisms related to breast cancer development, we investigated the role of HDAC2 in breast cancer and the inhibitory effect of miR-646 on this oncogene.
METHODS
A total of thirty cancerous tissues and 30 adjacent non-cancerous specimens and also three breast cancer cell lines were enrolled in the study. Quantitative reverse transcriptase PCR (qRT-PCR) was employed to detect the HDAC2 and miR-646 expression level in the studied samples. The biological roles of HDAC2 and miR-646 were investigated through manipulating the expression level of HDAC2 or miR-646 in breast cancer cells. Finally, we evaluated whether the HDAC2 is a direct target for miR-646.
RESULTS
In this study, we found HDAC2 is significantly upregulated in cancerous specimens and cell lines compared to non-cancerous tissues and normal cell line. On the other hand, miR-646 expression was decreased in clinical specimens and breast cancer cells compared to non-cancerous samples. Knocking out of the HDAC2 and overexpression of miR-646 inhibited breast cancer cell growth but promoted cell death, while untreated groups showed inverse results. Furthermore, we showed that in the breast cancer cells, miR-646 regulates the progression and proliferation by suppressing HDAC2.
CONCLUSION
Taken together, our study identified a miR-646/HDAC2 regulatory function in the breast cancer development and introduced a therapeutically target for breast cancer.
Identifiants
pubmed: 32777446
pii: S0890-8508(20)30300-5
doi: 10.1016/j.mcp.2020.101649
pii:
doi:
Substances chimiques
MIRN646 microRNA, human
0
MicroRNAs
0
HDAC2 protein, human
EC 3.5.1.98
Histone Deacetylase 2
EC 3.5.1.98
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
101649Informations de copyright
Copyright © 2020 Elsevier Ltd. All rights reserved.