KIFC1 (Kinesin Family Member C1)

These data collectively identify all five natural compounds as possible inhibitors of KIFC1. Nonetheless, their effectiveness and safety must be confirmed through in vivo and in vitro study prior to consideration for clinical application.

We show that TPX2 and KIFC1 cooperate to ensure robust acentrosomal microtubule nucleation and organization. Our data show that this mechanism plays a major role in the clustering of supernumerary centrosomes in cancer cells.

Collectively, these findings demonstrate that SSEO exerts cytotoxic effects primarily through the induction of apoptosis in both breast and lung cancer cells, highlighting its potential as a complementary anticancer agent. The online version contains supplementary material available at 10.1007/s13205-025-04656-0.

Overall, our findings shed light on the molecular mechanisms underlying chemoresistance in TNBC. This study provides compelling evidence supporting KPNA2 as a promising therapeutic target for overcoming chemoresistance in TNBC.

We have shown for the first time the molecular regulatory mechanism between KIFC1 and BUB1B on PC. Therefore, KIFC1 shows promise as an attractive therapeutic target for PC in the future.

ETV1 overexpression reversed the role of KIFC1 knockdown in inhibiting cell proliferation, invasion, migration, and EMT, as validated in vivo. KIFC1 serves as a tumor activator in pancreatic cancer by promoting proliferation, migration, invasion, and tumor growth, which may be partly manipulated by ETV1.

Conversely, the neutralization of both ADCY10 and KIFC1 through knockdown or pharmacological inhibition abrogates the oncogenic effects mediated by OLCarn. Hence, obesity-induced systemic environmental changes lead to the aberrant accumulation of OLCarn within the TME, making it a potential therapeutic target and biomarker for breast cancer.

MD simulations analysis showed minor variation in root-mean-square deviation and fluctuation, confirming their equilibrium with KIFC1 protein. The study enhances understanding of propolis compounds' inhibitory effects on KIFC1 protein, providing insights for potential treatment approaches and requiring further experimental (in vivo and in vitro) as well as clinical validation.

Inhibition of the MDR1 drug efflux pump restores taxol sensitivity in models characterized by ABCB1 overexpression. These MDR1-driven resistant models also respond to cabazitaxel, which is a poor MDR1 substrate, highlighting a potential therapeutic option for ovarian cancers with acquired taxol resistance.

Our results highlight the specificity and selectivity of in vitro generated CDK5RAP2 scaffolds and identify a minimal set of components required for human PCM assembly and function. This minimal model offers a powerful tool for studying centrosome biology and dysfunction in human health and disease.

Inhibiting KIFC1 using the small molecule inhibitor CW069 significantly reduced tumor volume in mice bearing AR-TNBC xenografts, but not in those with triple-negative breast tumors. These data suggest that upregulation of C/EBPβ and KIFC1 contributes to the aggressive characteristics and poor prognosis of AR-TNBC, providing strong evidence that targeting KIFC1 using kinesin inhibitors could be a viable therapeutic approach for patients with AR-TNBC.