YES1 (YES Proto-Oncogene 1, Src Family Tyrosine Kinase)

This initial systematic pan-cancer investigation establishes YES1 as a pleiotropic oncogenic regulator, with mechanistic heterogeneity across tumor lineages. The multidimensional characterization provides a translational framework for developing lineage-specific therapeutic strategies targeting YES1 signaling networks.

In conclusion, our study demonstrated that NSUN2 facilitated malignant proliferation and migration of PCa cells by enhancing YES1 mRNA stability via m5C modification. These findings suggested that both NSUN2 and YES1 may serve as potential therapeutic targets for PCa, offering new strategies for treatment.

Treatment with verteporfin reversed the alleviating effects of YES1 overexpression on neuronal DNA damage and exacerbated POCD in mice. In conclusion, bupivacaine induces POCD by suppressing YES1 expression and YAP1 phosphorylation, leading to DNA damage.

Treatment with dasatinib, a YES1 inhibitor, reduced cisplatin-induced cytotoxicity in UMUC-14 cells, suggesting that YES1 influences cisplatin efficacy in UC cells. Our findings indicate that YES1 plays a critical role in cisplatin resistance and may represent a promising therapeutic target in bladder cancer.

Consequently, CircINADL enhanced the stability of the HuR target gene Yes1-associated transcriptional regulator (YAP1), leading to the dysregulation of the Hippo signaling pathway. In conclusion, our study reveals the function of circINADL in promoting NPC metastasis and highlights its potential as a biomarker and therapeutic target for NPC treatment.

ACSL3 suppresses breast cancer progression by impeding lipid metabolism reprogramming, and inhibiting malignant behaviors through phospho-YES1 mediated inhibition of YAP1 and its downstream pathways. These findings suggest that ACSL3 may serve as a potential biomarker and target for comprehensive therapeutic strategies for breast cancer.

Mechanistically, mtiRL is found to specifically bind the oncoprotein Annexin A2 (ANXA2) to promote its Tyr24 phosphorylation by enhancing the interactions between ANXA2 and Yes proto-oncogene 1 (Yes1), leading to ANXA2 activation and increased p-ANXA2-Y24 nuclear localization in BC cells. Together, these findings define a critical role for mtiRL and suggest that targeting this novel m7G-modified tsRNA can be an efficient way for to treat BC.

SG can enhance hepatic regenerative capacity and improve liver metabolism. This study provides a better understanding of the mechanisms underlying SG-induced metabolic improvements.

Moreover, recent advances in targeted therapy for YES1-amplified malignancies are summarized. Finally, we conclude that targeting YES1 may reverse drug resistance and serve as a valuable tumor treatment strategy.

This interaction led to increased expression of YES1 and subsequent activation of downstream β-catenin signaling, thereby promoting ESC growth in Hu sheep. These findings provide novel molecular insights into the mechanisms underlying prolificacy in sheep.

In contrast, in EC-specific Src-deficiency, VE-cadherin internalization is maintained, and leakage is suppressed. In conclusion, Yes-mediated phosphorylation regulates constitutive VE-cadherin turnover, thereby maintaining endothelial junction plasticity and vascular integrity.

TP53, MAPK1, SOCS1, MBD3, and YES1 are the signature hub genes that might be responsible for the aggressive prognosis of PCL leading to poor survival rate. However, p53, MAPK1, and YES1 can be targeted with oxaliplatin, mitoxantrone, and ponatinib.