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A novel report of MiR‐4301 induces cell apoptosis by negatively regulating DRD2 expression in human breast cancer cells
Author(s) -
Gholipour Naghmeh,
OhradanovaRepic Anna,
Ahangari Ghasem
Publication year - 2018
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.26577
Subject(s) - skbr3 , apoptosis , flow cytometry , cancer research , cell growth , transfection , reverse transcription polymerase chain reaction , chemistry , cell culture , microbiology and biotechnology , mtt assay , microrna , breast cancer , biology , cancer , messenger rna , human breast , gene , biochemistry , genetics
In several cancers, microRNA (miRNAs) play vital roles in tumor initiation, drug resistance, and metastasis. The aim of this study was to examine the expression levels of miR‐4301 in human breast cancer and investigate whether its potential roles involved targeting Dopamine receptor D2 ( DRD2 ). Real‐time quantitative reverse transcription polymerase chain reaction (qRT‐PCR) was also used to examine the expression levels of miR‐4301 in human breast cancer cell lines MDA‐MB‐231, MCF‐7, and SKBR3. In these cell lines, MTT assay, immunofluorescence staining, caspase assay, proliferation assay, and flow cytometry were conducted to explore the potential functions of miR‐4301. The effects of modulating miR‐4301 on transcription levels of DRD2 were subsequently confirmed via qRT‐PCR. miR‐4301 expression levels were significantly decreased in human breast cancer specimens and cell lines ( P < 0.05). Transfection of miR‐4301 in breast cancer cells suppressed cell proliferation and induced apoptosis. Expression analysis indicated that miR‐4301 was inversely correlated with DRD2 expression in breast cancer specimens. qRT‐PCR showed that miR‐4301 negatively regulated DRD2 expression. Downregulation of DRD2 expression in MDA‐MB‐231, MCF‐7, and SKBR3 cells suppressed cell proliferation and promoted apoptosis.