In this study, OATP1B1 uptake function was found to be significantly suppressed by SRC proto-oncogene, non-receptor tyrosine kinase family kinase inhibitors, with SU6656 demonstrating the most potent inhibitory effect...Abrogation of Caveolin-1 exhibited no effect on the interaction between YES-1 and OATP1B1 but reduced the phosphorylation level of the transporter. Taken together, inhibitors of YES-1 may alter the uptake function of OATP1B1, potentially leading to drug-drug interactions related to post-translational modification.

This validated mitochondrial risk model delivers a clinically actionable biomarker for BLCA prognosis stratification and guides personalized therapeutic selection, enabling precision treatment intensification.

Drug sensitivity analysis identified BX-795 and tozasertib as potential treatments for tumors with high IGSF8 expression. Knockdown of IGSF8 significantly inhibited the proliferation ability of prostate cancer cells. Our findings indicated that IGSF8 might be used as a potential prognostic marker and therapeutic target for various cancers.

Mechanistic studies using immunoblotting, immunofluorescence staining, and flow cytometry showed that 9h outperforms ENMD-2076 in inhibiting Aurora A kinase activation, preventing spindle formation, arresting the cell cycle, and inducing cell apoptosis. Thus, 9h has the potential for further optimization and is a promising anticancer drug candidate.

P1/2, N=32, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Jun 2025 --> Jun 2026 | Trial primary completion date: Jun 2025 --> Jun 2026

Finally, cGBs-guided seven candidate drugs (Digitoxin, Camptosar, AMG-900, Imatinib, Irinotecan, Midostaurin, and Linsitinib) as the common treatment against T2D, CRC and HCC were identified through molecular docking, cross-validation, and ADME/T (Absorption-Distribution-Metabolism-Excretion-Toxicity) analysis. Most of these findings received support by the literature review of diseases specific individual studies. Thus, this study offers valuable insights for researchers and clinicians to improve the diagnosis and treatment of CRC and/or HCC patients during the co-occurrence of T2D.

Our study is the first to reveal that TAK-901 induces apoptosis in prostate cancer cells and inhibits cell growth by targeting EPHA2. These findings provide valuable insights into the underlying mechanisms of TAK-901 and may develop its therapeutic applications in prostate cancer.

Finally, dasatinib and tozasertib were identified as drug candidates capable of converting cold pancreatic adenocarcinoma tumors into hot tumors. In this study, we developed a framework for discerning clinically significant immune subtypes across various cancer types, further identifying several potential targets for converting cold tumors into hot tumors to enhance anticancer treatment efficacy.

Both docking studies revealed perfect binding of all identified ligands in active site pockets of AAK protein with similar amino acids of active sites as compared with standard BindingDB_50433632 compound and co-crystal ligand VX-680 binding mode of AAK protein. Therefore, it can be concluded that computational drug discovery approaches are meticulously implemented to identify potential AAKs inhibitors/modulators, and credential of the work was substantiated through the identification of three potential AAKs inhibitors/modulators that may hold significant promise for improving cancer management, however, need extensive biological assays or pre-clinical trials for assessing the efficacy profile of the identified compounds.

Similarly, compounds 28, 16, and 7 demonstrate strong AURK-B inhibitory activity, with IC50 values of 10.5 nM, 12 nM, and 14.09 nM, respectively. This comprehensive overview aims to support medicinal chemists in developing more potent, selective, and safe AURK inhibitors as potential anticancer therapeutics.

The IC50 values of predicted drugs, in the case of Tozasertib 1096 and WIKI4 1940, were significantly variant between risk groups...The study established an ARG prognosis model of ESCC. It provided a reference for the research of ARGs in ESCC.

Consistently, AURK inhibitors VX-680 (tozasertib), MLN8237 (alisertib), AZD1152-HQPA (barasertib) resulted in the upregulation of DYRK1B expression in A549 cells. In summary, our findings indicate that the expression of DYRK1A and DYRK1B is differentially regulated in cancer cells and reveal that the kinase inhibitor XMU-MP-1 increases DYRK1B expression likely through off target inhibition of Aurora kinases.