H-Index
79
Scimago Lab
powered by Scopus
JCR
Clarivate
Analytics
15%
Acceptance
Rate
call: +1.631.470.9640
Mon-Fri 10 am - 2 pm EST

Logo

Medical Science Monitor Basic Research
AmJCaseRep

Annals
ISI-Home

eISSN: 1643-3750

MiR-27a Modulates Radiosensitivity of Triple-Negative Breast Cancer (TNBC) Cells by Targeting CDC27

Yong-qiang Ren, Fengkui Fu, Jianjun Han

Clinical Laboratory, The Central Hospital of Yishui, Linyi, Shandong, China (mainland)

Med Sci Monit 2015; 21:1297-1303

DOI: 10.12659/MSM.893974

Available online:

Published: 2015-05-06


#893974

BACKGROUND: MiR-27a is significantly overexpressed in triple-negative breast cancer (TNBC). However, the exact biological function of MiR-27a in TNBC is not fully understood. In this study, we verified miR-27a expression in TNBC cells and explored how its overexpression modulates radiosensitivity of the cells.
MATERIAL AND METHODS: qRT-PCR analysis was performed to study miR-27a expression in TNBC lines MDA-MB-435 and MDA-MB-231 and in normal human breast epithelial cell line MCF10A. Dual luciferase assay was performed to verify a putative downstream target of miR-27a, CDC27. CCK-8 assay was used to assess the influence of miR-27a-CDC27 axis on cell proliferation under irradiation (IR) treatment.
RESULTS: We confirmed significantly higher miR-27a expression in 2 TNBC cell lines – MDA-MB-435 and MDA-MB-231 – than in human breast epithelial cell line MCF10A. miR-27a could modulate proliferation and radiosensitivity of TNBC cells. CDC-27 is a direct target of miR-27a and its downregulation conferred increased radioresistance of the cells.
CONCLUSIONS: The miR-27a-CDC27 axis might play an important role in modulating response to radiotherapy in TNBC cells. Testing miR-27a expression might be a useful way to identify a subgroup of patients who will benefit from an IR-based therapeutic approach.

Keywords: Binding Sites, Apc3 Subunit, Anaphase-Promoting Complex-Cyclosome - physiology, Breast - cytology, Cell Line, Tumor - radiation effects, Cells, Cultured, Conserved Sequence, Down-Regulation, Epithelial Cells - metabolism, Gene Expression Regulation, Neoplastic - drug effects, HEK293 Cells, MicroRNAs - physiology, Molecular Targeted Therapy, Neoplasm Proteins - physiology, Oligonucleotides - pharmacology, RNA Interference, RNA, Small Interfering - pharmacology, Radiation Tolerance - genetics, Recombinant Fusion Proteins - genetics, Reverse Transcriptase Polymerase Chain Reaction, Triple Negative Breast Neoplasms - radiotherapy, Tumor Stem Cell Assay



Back