Effects of KIF3A gene silencing and overexpression on proliferation, migration and invasion of human triple negative breast cancer cells

Abstract

Objective To study the effects of KIF3A silencing and overexpression on tumor proliferation, migration and invasion in human triple negative breast cancer (TNBC) cell lines. Methods With lentivirus-mediated interference technology made KIF3A gene silence in TNBC MDA-MB-231 cells, KIF3A gene was transfected into TNBC MDA-MB-468 cells bv liposome method. Subsequently, Western blotting analysis was performed to detect protein expression of KIF3A in these cells. Colony-formation assay, transwell migration and invasion assay were applied to estimate proliferation, migration and invasion ability of cells. Results The expression of KIF3A protein in the KIF3A-shRNA group cells was significantly silenced compared with those in the Scr-shRNA group cells. The expression of KIF3A in the KIF3A-pEX group cells was increased compared with those in the Vector group cells. The colony numbers in the KIF3A-shRNA group were significantly lower than those in Scr-shRNA group (174.8±46.26 vs. 293.2±20.93, P<0.01). The colony numbers in the KIF3A-pEX group were significantly higher than those in Vector group cells (292.00±75.59 vs. 151.40±68.58, P<0.05). The result of the transwell migrated assay showed that the numbers of migrated cells in the KIF3A-shRNA group were significantly lower than those in Scr-shRNA group (47.60±5.77 vs. 161.40±20.16, P<0.01) and the numbers of migrated cells in the KIF3A-pEX group were significantly higher than those in Vector group (262.00±23.35 vs. 155.00±29.15, P<0.01). It was confirmed via the transwell invasion assay results that the cell’s invasive ability of KIF3A-shRNA group was progressively suppressed as compared with the Scr-shRNA group (161.40±16.16 vs. 281.00±19.77, P<0.01) and the cell’s invasive ability of KIF3A-pEX group was progressively promoted as compared with the Vector group (214.00±34.54 vs. 125.40±19.94, P<0.01). Conclusion Down-regulation of KIF3A in TNBC cell can inhibit the cell proliferation, migration and invasion. Overexpression of KIF3A in TNBC cell can promote the cell proliferation, migration and invasion. KIF3A might hold potential as a therapeutic drug target for human TNBC. Key words: KIF3A; Short hairpin RNA; Triple negative breast cancer; Proliferation; Migration; Invasion