CDC25B (Cell Division Cycle 25B)

This study, for the first time, validated the antitumor effect of farrerol against CRC through network pharmacology, molecular docking, molecular dynamics simulations, and in vitro experiments. The findings indicate that the ability of farrerol to inhibit the proliferation and migration of colorectal cancer cells may be associated with the induction of G0/G1 phase cell cycle arrest and the regulation of VEGF signaling pathway activation via binding to VEGFA and KDR.

This analysis of a phase II randomized trial included patients with gastric adenocarcinoma treated with Menadione plus XELOX or XELOX alone. PFS analysis showed a higher risk of progression in No-CTC responders, with HRs of 2.28 at 3 months and 10.5 at 15 months (p < 0.001). Patients without CTC response had worse OS and PFS in both treatment groups, suggesting that CTC response could be a valuable predictor of clinical outcomes, warranting more intensive monitoring and tailored therapies for specific subgroups.

Three critical CRC-affecting genes were identified, offering new molecular insights and potential research and treatment directions.

α-hederin may be an effective drug to inhibit cervical cancer and has a good development prospect.

We identified key APIGs and constructed a robust APIG-based prognostic signature for HCC. CDC25C was a key target through which APs impact HCC and multiple other cancers.

MO-A can impede ESCC growth by triggering cell cycle G2/M arrest, posi-tioning it as a novel and promising phytocompound for ESCC therapy.

Pathway enrichment analysis highlighted KRAS, ESR1, ESR2, RAB10, TNRC6C, and NCAN as the most commonly differentially expressed in EA, whereas ERBB4, PLCB1, and SERPINE1 were most frequently in AA. These findings highlight the importance of considering race-specific miRNA-mRNA signatures in understanding TNBC in the context of obesity, offering insights into biomarker-driven patient stratification for targeted therapeutic strategies.

Additionally, variations in IER5 levels led to differences in the expression levels of p53, NF-YB, and p300, which may be putative transcriptional regulators of Cdc25B. These results suggest that IER5 plays a negative role in regulating Cdc25B expression, which may involve interactions with the transcriptional regulators p53, NF-YB, and p300.

CDC25B is highly expressed in sarcoma, and blocking of CDC25B can suppress sarcoma progression by inducing G2 cell cycle arrest. These findings suggest that CDC25B may serve as a potential molecular biomarker and therapeutic target for sarcoma.

In vivo studies in xenograft mice showed that 15 mg/kg FPP29 inhibited tumor growth by 75 % with no apparent toxicity. Collectively, FPP29 exhibits strong anti-cancer effects in vitro and in vivo, highlighting its promise as a lead compound for FOXM1-targeted therapeutic development with favorable safety profiles.

Docking with CDC25B showed that rosmarinic acid also binds in the same place as cyclin-dependent kinases (CDKs). The ability of rosmarinic acid to inhibit MMP-1, MMP-2, MMP-9, aldose reductase, and CDC25B activity may underlie how rosmarinic acid is able to inhibit the development of breast cancer.

Based on potency and drug-ability, we have selected 'CDK1-naringenin' with the standard drug complex, 'CDK1-dinaciclib,' for molecular dynamic simulation at 100 nanoseconds using GROMACS 2020 software. Based on potency (average docking score: 8.35 kcal/mol.), physicochemical properties (obeyed Lipinski rule of five), toxicity (class-IV), fifty percent lethal dose (2000 mg/kg), bioavailability (0.55), drug-likeness score (0.82), along with ideal pharmacokinetics profiles and higher protein-ligand stability, naringenin is considered as a potential and non-toxic anticancer candidate to be used for melanoma as alternative or complementary agent. The integrative and systematic analyses not only highlight the potential of phytoflavonoids but also select the potential lead from the library within limited resources to accelerate the current anticancer drug discovery process.