To determine if FANCF can serve as a novel therapeutic target for breast cancer, we first used shRNA to knock down FANCF expression in breast cancer cells.
To observe the effect of FANCF shRNA on the FA/BRCA pathway function, we detected the level of FANCD2 ubiquitination at 48 h after transfection.
Silencing of FANCF inhibited cell proliferation in breast cancer cells
To determine whether FANCF shRNA actually affects proliferation of breast cancer cells, we examined the proliferation of MCF-7 cells and MDA-MB-435S cells (normal FANCF expression) in response to FANCF shRNA treatment.
Silencing of FANCF enhanced DNA damage in breast cancer cells
Since FANCF plays important roles in DNA damage repair (27), we thus assessed the effect of FANCF shRNA on DNA damage using the alkaline comet assay.
Silencing of FANCF induced cell cycle arrest (S arrest) and apoptosis in breast cancer cells
The effect of FANCF shRNA on the cell cycle was studied by flow cytometry.
It was observed that FANCF shRNA increased the percentage of cells undergoing apoptosis compared to the untreated cells or control shRNA treated cells (P<0.05; Figure 5).
Silencing of FANCF decreased cell invasion and migration in breast cancer cells
We next investigated whether silencing of FANCF could influence invasion and migration.
Silencing of FANCF resulted in increased chemosensitivity to Dox in breast cancer cells