Fig 1: ARL6IP5 inhibited cellular proliferation, invasion, migration, and adhesion in OC and CisR OC cells.A CisR cells were generated from OC cells via gradual increments of cisplatin treatment for 8 months. Cell viability and IC50 of OC and CisR OC cells following exposure to cisplatin were determined. The IC50 of the resulting CisR cells were over five times greater than the parental OC cells. B OC and CisR OC cells were transfected with empty vector, si-NC (for negative control), pcARL6IP5 (ARL6IP5 + + ; for overexpression), and si-ARL6IP5 (for knockdown). Effects of ARL6IP5 overexpression and knockdown on cellular C proliferation, D invasion, E migration, F adhesion in OC and CisR OC cells (original magnification, ×10; scale bar, 100 µm). *p < 0.05 compared with empty vector; #p < 0.05 compared with si-NC.
Fig 2: ARL6IP5 expression significantly reduced cisplatin-resistance and significantly decreased DNA repair protein expression.A Cell viability and IC50 of OC and CisR OC cells transfected with empty vector, si-NC, pcARL6IP5 (ARL6IP5 + + ; for overexpression), and si-ARL6IP5 (for knockdown) following exposure to cisplatin. B Expression of DNA repair-related proteins to determine the effect of ARL6IP5 overexpression and knockdown were analyzed by western blots. *p < 0.05 compared with empty vector; #p < 0.05 compared with si-NC.
Fig 3: ARL6IP5 inhibited wound healing and apoptosis in OC and CisR OC cells.OC and CisR OC cells were transfected with empty vector, si-NC, pcARL6IP5 (ARL6IP5 + + ; for overexpression), and si-ARL6IP5 (for knockdown). Effects of ARL6IP5 overexpression (ARL6IP5 + + ) and knockdown (si-ARL6IP5) on A wound healing and B apoptosis in OC and CisR OC cells. A Wound-healing assay was performed to detect the composite adhesion and migration abilities of OC and CisR OC cells. Time-lapse microscopy images of wound closure; dotted lines define the area lacking the cells (original magnification, ×10; scale bar, 100 µm). Quantification of the invaded wounded area after 12 h expressed as the percentage of gap area at 0 h. B Apoptosis assay of OC and CisR OC cells transfected with empty vector, si-NC, pcARL6IP5 (ARL6IP5 + + ) and si-ARL6IP5. Cells were treated with 50 or 100 µM of cisplatin, and the apoptotic rates were analyzed 24 h after cisplatin treatment (original magnification, ×20; scale bar, 50 µm). *p < 0.05 compared with empty vector; #p < 0.05 compared with si-NC.
Fig 4: ARL6IP5, XRCC1, and PARP1 protein expression was low-throughout OC cell lines compared to normal ovarian epithelial cell.ARL6IP5, XRCC1, and PARP1 expression was analyzed by western blots in 8 OC cell lines, ES-2, OV-90, TOV21sG, CaOV-4, CaOV-3, TOV112D, SKOV3, OVCAR-3, and one normal ovarian cell line, Hs823.Tc.
Fig 5: ARL6IP5 expression significantly reduced cisplatin-resistance and significantly increased pro-apoptotic protein expression.Expression of apoptosis-related proteins in the A extrinsic and B intrinsic pathways to determine the effect of ARL6IP5 overexpression and knockdown were analyzed by western blots. *p < 0.05 compared with empty vector; #p < 0.05 compared with si-NC.
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