Cell cycle distribution analysed by flow cytometry and ModFit after 72 hours of treatment with increasing concentrations of paclitaxel in (A) H-Scramble/H-shKIF26B cellsand (B) H-Scramble/H-shKIF26B cells. Proportions of cells in the G0/G1, S, and G2/M phases after exposure to varying paclitaxel concentrations for 72 hours.

Ovarian cancer, the most lethal tumour of the female reproductive system, severely threatens women’s life and health.Despite being a cornerstone of ovarian cancer chemotherapy, paclitaxel resistance eventually develops in most patients, posing a major therapeutic challenge. KIF26B, a kinesin family protein, is involved in various cancers, but its role in ovarian cancer and chemotherapy resistance is unclear.To further elucidate the cellular mechanisms underlying the increased paclitaxel sensitivity induced by KIF26B knockdown, flow cytometry was used to analyse cell cycle progression in both the H and H-R cell lines.H-shKIF26B, H-Scramble, H-R-shKIF26B, and H-R-Scramble cells were seeded in 6 cm culture dishes and treated with various concentrations of paclitaxel for 72 hours, with three replicates per group.Propidium iodide (PI) was used to assess distribution across the G0/G1, S, and G2/M phases.ModFit software was used to process the cell cycle data.Cell cycle distribution analysed by flow cytometry and ModFit after 72 hours of treatment with increasing concentrations of paclitaxel in H-Scramble/H-shKIF26B cells and H-Scramble/H-shKIF26B cells. Proportions of cells in the G0/G1, S, and G2/M phases after exposure to varying paclitaxel concentrations for 72 hours.