CDK3 (Cyclin Dependent Kinase 3)

Consistently, low CDKN3 expression in head and neck SCC occurs exclusively in female patients and correlates with better prognosis. We thus reveal a mechanism protecting women from carcinogen-induced cancer formation, which could lead to better sex-targeted preventive and therapeutic strategies in SCC.

5 prognosis-relevant LRGs could provide a novel perspective for the individualized therapeutic regimens for LUAD.

Vorinostat and raloxifene exhibited notable binding affinity for PEBP1. Furthermore, an independent prognostic model for LUAD was developed, enhancing our understanding of high-/low-risk cohorts' functional pathways. Drug prediction results provided valuable insights into potential therapeutic strategies for LUAD, warranting further investigation.

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.

In vitro, CCNB1 knockdown triggered cell cycle arrest, thereby suppressing the proliferation of colorectal cancer cells. This study validated CCNB1 as a dual-purpose biomarker for CRC diagnosis and favorable prognosis, highlighting its potential utility in clinical management.

Molecular docking analyses further supported these findings by demonstrating strong binding affinities of phytochemicals to key cell cycle regulatory proteins, suggesting a direct molecular basis for their antiproliferative effects. In conclusion, the n-butanol fraction of Ardisia villosa displays potent anticancer activity, particularly in gastric cancer cells, through multi-targeted mechanisms involving cell cycle inhibition and senescence induction, and holds promise as a natural source for future anticancer therapeutics.

PANI provides precise prognosis and immunotherapy response predictions for ccRCC patients, facilitating individualized treatment strategies.

CDKN3 was an oncogene whose overexpression promoted the initiation and progression of TNBC by inhibiting HSP90-mediated ferroptosis.

DOCK3 drives PCa metastasis through cytoskeletal dynamics while paradoxically promoting an immunologically active microenvironment. Its tumor-specific expression and association with aggressive clinical features nominate DOCK3 as a novel biomarker for risk stratification and a promising therapeutic target for combinatorial immunotherapy in immunologically "cold" PCa.

Owing to the fact that the Editorial Office has been made aware of potential issues surrounding the scientific integrity of this paper, we are issuing an Expression of Concern to notify readers of this potential problem while the Editorial Office continues to investigate this matter further. [Oncology Reports 31: 1825‑1831, 2014; DOI: 10.3892/or.2014.3045].

Targeting CDKs, particularly CDK3 and CDK4/6, may represent a promising therapeutic strategy for PCa.

Docking studies identified interactions of the five selected candidates with crucial residues of CDK3. Global reactivity suggested favourable electronic properties for receptor binding. MD simulations, MM-PBSA and ONIOM revealed stable ligand-receptor interactions and favourable binding energetics. Extended 1200ns simulations of the two hits, CID_11212010 and CID_25211747, demonstrated exceptional stability of CID_25211747 with minimal conformational fluctuation. Additional ONIOM calculations reproduced the strong binding affinity of CID_25211747 with CDK3. Collectively, these results nominate CID_25211747 as a promising lead towards the development of effective CDK3 antagonists, offering valuable insight for future drug design.