HOXB7-S3 inhibits the proliferation and invasion of MCF-7 human breast cancer cells.

Mol Med Rep

Department of Oncology, Zhongnan Hospital of Wuhan University, Hubei Cancer Clinical Study Center, Key Laboratory of Tumor Biological Behavior of Hubei, Wuhan, Hubei 430071, P.R. China.

Published: October 2015

Homeobox B7 (HOXB7) has been found to be overexpressed in numerous types of human cancer. However, the role of HOXB7 in breast cancer remains to be elucidated. The aim of the present study was to investigate the effects of HOXB7 on the proliferation and invasion of breast cancer cells. Initially, reverse transcription quantitative polymerase chain reaction and western blotting were respectively employed to detect the mRNA and protein expression levels of the HOXB7 gene in the MDA‑MB‑231 and MCF‑7 human breast cancer cell lines. Subsequently, small interfering RNAs designed to interfere with the expression of HOXB7 were used to knockdown the expression of HOXB7 in the MCF‑7 cell line, the effects of which on cell proliferation, the apoptotic rate and invasion capacity were measured using a Cell Counting kit‑8 assay, flow cytometry and transwell chambers, respectively. The results demonstrated that HOXB7 mRNA and protein were all overexpressed in MDA‑MB‑231 and MCF‑7 breast cancer cell lines. Furthermore, HOXB7‑S3 effectively inhibited the proliferation and invasion of MCF‑7 breast cancer cells. In conclusion, these results demonstrated that HOXB7 may be a potential therapeutic target in human breast cancer.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4581815PMC
http://dx.doi.org/10.3892/mmr.2015.4009DOI Listing

Publication Analysis

Top Keywords

breast cancer
28
proliferation invasion
12
human breast
12
cancer cells
12
cancer
8
hoxb7
8
mrna protein
8
mda‑mb‑231 mcf‑7
8
cancer cell
8
cell lines
8

Similar Publications

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!