FOXM1 (Forkhead Box M1)

Moreover, a positive correlation between FOXM1 and CBS expression was identified in lung cancer. Taken together, our results indicate that Brusatol functions as a novel FOXM1 inhibitor and inhibits lung cancer progression by blocking the activation of the FOXM1/CBS signaling axis.

Here, we mainly review and discuss our current molecular understanding of the mechanisms through which FOXM1 in cancer cells executes these new roles, and thereby induces therapy resistance and inhibits apoptosis in a variety of human cancers. We also discuss the opportunity and challenges for therapeutically targeting FOXM1 to induce apoptosis in drug-resistant cancers.

Inhibition of the FoxM1/Snail/EMT pathway reversed PKMYT1-induced metastasis in mice. Collectively, our findings identify the PKMYT1/FoxM1/Snail axis as a driver of ccRCC metastasis via EMT induction, highlighting PKMYT1 as a potential therapeutic target for ccRCC.

Strategic structural modifications significantly enhance the potency, selectivity, and pharmacokinetics of anti-TNBC agents. Future research should emphasize polypharmacology, advanced delivery strategies, and translational validation to address TNBC heterogeneity.

Reduction of these proteins pharmacologically or by siRNA knockdown greatly impairs the viability, colony formation, and proliferation of the FOXM1i-resistant cells, with lesser impact on CDK4/6i resistant cells. Notably, CDK4/6i resistant cells and 3D-Matrigel cultures can still be growth inhibited by FOXM1i, and conversely the FOXM1i resistance can be overcome by palbociclib or abemaciclib, indicating that while the resistance mechanisms of these two classes of drugs have some similar features, they are sufficiently distinct so that sequential treatment approaches could be effective in supporting new options such as FOXM1 inhibitor use after progression on CDK4/6 inhibitors.

Effect size estimates were relatively large for both the group effect (partial η2=0.20) and the time x group interaction (partial η2=0.24), suggesting that the study may have been underpowered to detect this difference statistically. In conclusion, the present exploratory study suggests that suramin exerts a dual antitumor effect on tongue squamous cell carcinoma by suppressing proliferative transcriptional programs, and modulating extracellular and stress response pathways, providing a basis for future studies to further elucidate its therapeutic relevance.

Nicotinamide metabolism was found to be significantly linked with EC progression. This study offers new perceptions into the role of nicotinamide metabolism in EC and suggests possible avenues for treatment advancements.

Our laboratory recently identified the actin-binding protein advillin (AVIL) as being overexpressed, oncogenic, and necessary for tumorigenesis in GBM. Here, we further examined AVIL expression in GBMs and found that it was enriched across molecular subtypes and states, including GBM stem cells and temozolomide-resistant samples...In summary, we have identified an efficacious first-in-class compound targeting an oncogene in GBM. Further optimization of the molecule may offer an effective therapeutic intervention for GBM.

TCGA-based analyses confirmed overexpression and hypomethylation of E2F3 and FOXM1 in breast cancer, particularly in triple-negative tumors, and high expression of both genes was associated with poor survival. These findings indicate that time-dependent loss of miR-548c-3p contributes to E2F3 and FOXM1 activation through a post-transcriptional regulatory mechanism, highlighting this miRNA-oncogene axis as a potential prognostic signature and therapeutic target in breast cancer.