CDK1 (Cyclin-dependent kinase 1)

Furthermore, PMLE treatment significantly activated p53 in A549 cells, followed by increased nuclear translocation, which may account for the up regulation of p16INK4a, p21Cip1, and p27Kip1 proteins. Taken together, our results indicate that PMLE exerts anti-cancer activity in human lung adenocarcinoma by arresting the cell cycle through activation of the p53-dependent pathway.

Critically, pharmacological inhibition of CDK1 completely abrogates the oncogenic phenotypes conferred by PPP1R14C. Our findings delineate a novel and actionable KLF7-PPP1R14C-PP1-CDK1 signaling cascade essential for LUSC pathogenesis, positioning PPP1R14C as both a prognostic biomarker and a compelling therapeutic target.

Molecular docking demonstrated the presence of affinity between target hub proteins and active compounds. This study revealed that SWT might exert its therapeutic effects on ESCC through multi-targets and multi-mechanisms.

Our finding that the antitumor activity of locally induced PF4 contrasts with its reported protumor effects when expressed systemically clarifies the context-dependent duality of PF4 in cancer. These results position TLR8 agonists as promising candidates for combination immunotherapy.

KM-Survival Analysis is depicted through Hazard Ratio (HR) and p-value identification. Drug-Target Docking Analysis of ligand molecule Hyaluronic Acid and drugs 5-Fluorouracil and Epirubicin and TCGA Drug Survival Analysis and Response are implicated for therapeutic interventions.

We further demonstrated in vivo that AC098613.1 overexpression significantly inhibited tumor growth by affecting the stability of CDC5L and regulating the expression of ADAP1, NRD1 and cyclin-dependent kinase 1 (CDK1). The research demonstrates that AC098613.1 promotes AML cell differentiation by regulating the CDC5L/ADAP1/NRD1 axis, providing a new target for AML differentiation therapy.

Subsequent SHAP analysis revealed SRC, HSP90AB1, HSP90AA1 and CDK1 as the key contributors to prognostic prediction, with each being highly expressed in BC and linked to poor clinical prognosis. Notably, among all chemicals screened, Disperse Yellow 3 exhibited the strongest binding affinity to these four key targets, demonstrating the strongest association with BC risk.

DEHP may promote the development of BLCA by interacting with key proteins and signaling pathways. This study provides a theoretical basis for understanding the molecular mechanisms of DEHP-induced BLCA and offers references for future prevention and treatment strategies.

The hinge-binding carboxamide cyclized derivative B3 demonstrated potent enzymatic inhibition (IC50 = 3.5 nM) and cellular CDK1 phosphorylation suppression (IC50 = 65-114 nM), selectively inhibited proliferation of CCNE1-amplified cancer cells (IC50 = 0.56-0.88 μM) through induction of γH2AX accumulation. Furthermore, compared to the first-in-class PKMYT1 inhibitor RP-6306, B3 exhibited enhanced solubility (176 vs 45 μM) and favorable in vivo metabolic stability (mouse clearance 58.2 vs 85.7 mL/min/kg), underscoring cyclization as a productive design strategy to improve drug-likeness of PKMYT1 inhibitors.

Furthermore, apigenin and Salvia coccinea promote hypoglycemic effect by attenuating α-amylase activity, cholesterol levels, insulin resistance, DRP1 expression by improving GLUT4, GSK-3β, AMPK/PI3K/Nrf2, and Akt pathways. Moreover, Salvia coccinea regulates wound healing after infection, injury, or surgery, in addition to improving agricultural productivity by reducing rodent attacks.

These modifications in the activation status of cDC1- and cDC2-like cells after tumor cell contact subsequently resulted in significantly enhanced CD8+ and CD4+ T cell proliferation. Current glioblastoma cell treatment impacts on the subsequent activation of cDCs and T cells and should serve as basis for improving immunotherapeutic strategies of brain tumors.

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.