Abstract
The aim of the current study was to evaluated the effect of BRCA1(breast cancer 1 early
0nsent) after UV-B-irradiation in a panel of human malignant melanoma cells using flow
cytometry method. Different human melanoma cell lines (SK-MEL28,SK-MEL93, ,SK
MeL93/shBRCA1 and SK-Mel93/shplKO.1) were cultured for triplicaten experiments. Cells
were exposed to UV-B (10mJ/cm2)for different point time(1/2,1,3,6,9,12,and 24h). Cells at
0hr were a non-irradiation control. The cell cycle was evaluated by flow cytometry. SK
MEL28 cell line seemed to be synchronized at the G1/S boundary phase until 12h after UVB
irradiation. a decrease in the fraction of S cells and a reciprocal increase of cells in Sub-G1
phase was observed , from 12 to 24h.While, the SK-MEL93 a rapid increase (about 35%) of
cells in Sub-G1 phase was observed already 6h after UVB irradiation. Moreover, we found
that the SKMel93/shBRCA1 cells seemed an increase (about 15%) of cells in Sub-G1 phase
already 12h after UVB irradiation compared with cells infected with the empty lentiviral
vector (SK-Mel93/shplKO.1). we conclude that an important role played by BRCA1
providing new insights into the molecular mechanisms underlying UV-induced
melanomagenesis.
0nsent) after UV-B-irradiation in a panel of human malignant melanoma cells using flow
cytometry method. Different human melanoma cell lines (SK-MEL28,SK-MEL93, ,SK
MeL93/shBRCA1 and SK-Mel93/shplKO.1) were cultured for triplicaten experiments. Cells
were exposed to UV-B (10mJ/cm2)for different point time(1/2,1,3,6,9,12,and 24h). Cells at
0hr were a non-irradiation control. The cell cycle was evaluated by flow cytometry. SK
MEL28 cell line seemed to be synchronized at the G1/S boundary phase until 12h after UVB
irradiation. a decrease in the fraction of S cells and a reciprocal increase of cells in Sub-G1
phase was observed , from 12 to 24h.While, the SK-MEL93 a rapid increase (about 35%) of
cells in Sub-G1 phase was observed already 6h after UVB irradiation. Moreover, we found
that the SKMel93/shBRCA1 cells seemed an increase (about 15%) of cells in Sub-G1 phase
already 12h after UVB irradiation compared with cells infected with the empty lentiviral
vector (SK-Mel93/shplKO.1). we conclude that an important role played by BRCA1
providing new insights into the molecular mechanisms underlying UV-induced
melanomagenesis.