Objective: To observe the effects of metastasis-associated tumor gene family 2 (MTA2) depletion on humanbreast cancer cell proliferation and metastasis.
Methods: A short-hairpin RNA targeting MTA2 was chemicallysynthesized and transfected into a lentivirus to construct Lv-shMTA2 for infection into the MDA-MB231human breast cancer cell line. At 48 hours after infection cells were harvested and mRNA and protein levels ofMTA2 were determined by quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting,respectively. Cell viability and metastasis were assessed by CCK-8, wound-healing assay and Transwell assay,respectively. In addition, a xenograft model of human breast cancer was constructed to investigate cancerouscell growth and capacity for metastasis.
Results: After infection with Lv-shMTA2, mRNA and protein levelsof MTA2 was significantly reduced (p<0.05) and MDA-MB231 cell proliferation and metastasis were inhibited(p<0.05). In addition, mean tumor size was smaller than that in control group nude mice (p<0.05) and numbersof metastatic deposits in lung were lower than in control group mice (p<0.05). Depletion of MTA2 affectedMMP-2 and apoptosis-related protein expression.
Conclusions: For the first time to our knowledge we showedthat MTA2 depletion could significantly inhibit human breast cancer cell growth and metastasis, implying thatMTA2 might be involved in the progression of breast cancer. The role of MTA2 in breast cancer growth andmetastasis might be linked with regulation of matrix metalloproteinase and apoptosis.