CDKN1A (Cyclin-dependent kinase inhibitor 1A)

Of these agents, Telomelysin (OBP-301, Suratadenoturev), a telomerase-specific oncolytic adenovirus, demonstrated clinical safety but limited efficacy in refractory tumors. Given its multifaceted antitumor functions and ability to overcome key barriers in pancreatic cancer, OBP-702 represents a highly promising therapeutic candidate. A first-in-human clinical trial evaluating endoscopic ultrasonography-guided intratumoral injection of OBP-702 is currently in preparation, expected to advance clinical translation of this novel virotherapeutic strategy.

Our findings indicate that periplogenin suppresses hepatocarcinogenesis by inducing cellular senescence through activation of the FOXO1/P53 pathway. These results highlight the potential of periplogenin as a novel therapeutic agent for the treatment of hepatocellular carcinoma.

To investigate oxaliplatin (OXA)‑induced senescence in GC cells, cellular senescence was assessed by senescence‑associated β‑galactosidase (SA‑β‑Gal) staining, western blotting, immunofluorescence, and reverse transcription‑quantitative polymerase chain reaction for the senescence‑associated secretory phenotype (SASP) factors...The present study identified NR4A1 as a key regulated gene in chemotherapy‑induced senescence in GC and verified that the NR4A1/AKT‑metabolism axis is vital for the pivotal mechanism of TIS. These findings may provide a novel therapeutic strategy to optimize chemotherapy and develop 'one‑two punch' approaches targeting senescent tumor cells.

Molecular docking showed that TMEM119 exhibited strong binding affinity for Danazol, Drospirenone, and Sufugolix. Collectively, TMEM119 is significantly upregulated in ovarian EM, where it blocks ectopic endometrial stromal cell senescence via MAPK signalling and consequently accelerates lesion expansion. Inducing cellular senescence may therefore constitute a tractable therapeutic avenue for ovarian EM.

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.

In MDA-MB-231 xenografts, compound 30 significantly inhibited tumor growth in a dose-dependent manner without observable toxicity. These findings highlight compound 30 as a promising therapeutic candidate for TNBC treatment through CSN5 inhibition, which simultaneously induces PD-L1 degradation and direct antitumor activity.

We observed no evidence of established stress-induced premature or replicative senescence in drug-resistant epilepsy patients. However, elevated proinflammatory cytokines and high p21/p16 expression in the drug-resistant group may suggest ongoing seizures cause cellular stress which could increase susceptibility to senescence in drug-resistant pediatric epilepsy patients over time.

We critically discuss the pivotal role of miR-302/367 cluster in pluripotency and reprogramming while countering aging hallmarks. Finally, we explore how combining single-miRNA therapeutics with clinically viable delivery systems (lipid nanoparticles and extracellular vesicles) can link cellular reprogramming with targeted rejuvenation therapies.

TNFSF4 was a candidate driver and a prognostic biomarker, promoting HCC progression by activating the PI3K/Akt signaling pathway. Furthermore, fluspirilene may have applications as a repositioned drug for HCC with high TNFSF4 expression.

In parallel, the transfection of tumour cells with pure synthetic miR160b-5p-a microRNA identified in M. sylvestris flowers and predicted to target the human CDK2 transcript-resulted in gene silencing, thereby suggesting its central role in mediating the cross-kingdom effects of MFE on the investigated cancer models. Overall, these findings open new perspectives on the common mallow as a source of potential antimetastatic compounds and on the possible use of its plant microRNAs in the development of gene therapies.

We identified three new major downstream targets of Snail1 that improve our understanding of the role of EMT in limiting stress signaling, apoptosis, and senescence during cell cycle suppression to create a vulnerability for therapeutic targeting.

PTX3 and IL-6 are potential biomarkers of disease severity and prognosis. Targeting inflammaging pathways could offer new therapeutic strategies for RCC, particularly in aggressive disease forms.