Pasarat Khongkow

TL;DR: It is suggested that paclitaxel targets the FOXM1-KIF20A axis to drive abnormal mitotic spindle formation and mitotic catastrophe and that deregulated FoxM1 and Kif20A expression may confer paclitAXel resistance.

TL;DR: It is found that SIRT6 protein levels are elevated in paclitaxel- and epirubicin-resistant MCF-7 cells compared with the parental sensitive cells, and cell viability studies demonstrate that deletion of FOXO1/3/4 in MEFs can confer sensitivity to both pac litaxel and epIRubic in, suggesting that Sirt6 reduces paclitaxeel andEpirubICin sensitivity, at least in part, through modulating FOXO

TL;DR: It is suggested that FOXM1 increases NBS1 expression and ATM phosphorylation, possibly through increasing the levels of the MRN(MRE11/RAD50/NBS1) complex, and the DNA repair-defective and senescence phenotypes inFOXM1-deficent cells can be effectively rescued by overexpression of NBS 1.

TL;DR: Co-immunoprecipitation experiments demonstrated that FOXM1 expression is associated with OTUB1 binding but inversely correlates with conjugation to the protein degradation-associated Lys-48-linked ubiquitin-chains, and Cox-regression survival analysis indicates that OTUB 1 overexpression is linked to poorer outcome in patients treated with chemotherapy.

TL;DR: It is shown that FOXM1-overexpressing breast cancer cells display an apoptosis-resistant phenotype, which associates with the upregulation of expression of XIAP and Survivin antiapoptotic genes, which contributes to the development of drug-resistance and is associated with poor clinical outcome in breast cancer patients.