YAP1 overexpression

Pharmacological inhibition of Casein kinase II by Silmitasertib or genetic depletion of the catalytic subunit of Casein kinase II (CK2α) markedly destabilizes YAP1 and consequently suppresses its oncogenic functions in vitro and in vivo...Notably, upregulated expressions of CK2α and DUB3 in ovarian cancer positively correlate with YAP1 overexpression. Collectively, our findings demonstrate the functional significance of the CK2α-DUB3 axis in YAP1 stabilization and YAP1-driven tumor progression, highlighting that strategies to target this axis might be of benefit in the clinical management of ovarian cancer and several other lethal cancers with aberrantly upregulated YAP1.

Regarding "druggable markers," DLL3 was expressed in 66% of tumors and PD-L1 in 17.4%. Detailed analyses of different prognostic and predictive markers are needed to better understand EP-SCNC biology and create more personalized therapy to improve patient prognosis.

LAMA3 knockdown promotes CC sensitivity to oxaliplatin via modulating the Hippo-YAP pathway, providing new therapeutic targets for the CC treatment.

YAP1 is a potential novel prognostic marker in ACC patients. Its deregulation contributes to adrenocortical tumorigenesis partially through crosstalk between Hippo/YAP1 and Wnt/beta-catenin pathways. YAP1 inhibition is a new antitumor target.

The present study demonstrated that YAP1 positively regulates aerobic glycolysis by inhibiting EGLN2 expression, which results in an increased HIF-1α protein level and transcriptional activity. YAP1 was positively regulated and significantly correlated with HIF-1α-targeted glycolytic genes, including glucose transporter type 1(GLUT1), hexokinase2 (HK2) and lactate dehydrogenase A (LDHA). Elevated YAP1 expression and concomitant downregulation of EGLN2 contributed to poor survival in patients with pancreatic cancer. Our results suggest that YAP1 may be a promising predictive marker and treatment target for human pancreatic cancer.

Our research reveals that RNF6 is highly expressed in CC, driving malignant progression by upregulating YAP1 protein expression and enhancing the transcription of downstream target genes CTGF and CYR61, offering potential therapeutic targets for CC treatment.

Several studies have demonstrated that YAP1 is overexpressed in bladder cancer and is involved in adverse outcomes such as bladder cancer occurrence, progression, resistance to cisplatin and the recurrence of tumours...In addition, this study further explored the potential of YAP1 in the diagnosis and treatment of bladder cancer. This study aimed to explore the potential mechanism of YAP1 in the treatment of bladder cancer.

PLOD2 exerted pro‑oncogenic effects on CESC through the p53 pathway by binding to YAP1. These findings provide new perspectives for the future study of PLOD2‑targeted therapy for CESC.

In vivo studies also confirmed that GL-V9 exerts anti-tumor effects by suppressing YAP1 expression, while also activating autophagy and inducing mitochondrial apoptosis in BXPC-3-bearing BALB/c nude mice. Our findings underscore the importance of autophagy-mediated YAP1 degradation in PDAC, providing a novel molecular rationale (GL-V9) as a promising treatment for this disease.

Overexpression of OTUD5 in gastric cancer cells partly reversed the anti-tumor effect of dapagliflozin. Our findings revealed a novel mechanism by which dapagliflozin has an antitumor effect on gastric cancer and proposed a beneficial strategy for the application of dapagliflozin in gastric cancer patients.

Finally, DHA reduced GLUT1-aerobic glycolysis in HCC cells through YAP1 and prevented the binding of YAP1 and HIF-1α. Collectively, our study revealed the mechanism of DHA inhibiting glycolysis in HCC cells from a perspective of a positive feedback loop involving YAP1 and GLUT1 mediated-aerobic glycolysis and provided a feasible therapeutic strategy for targeting enhanced aerobic glycolysis in HCC.

YAP1 knockdown also reduced the IC50 value following treatment with vincristine, daunorubicin, cyclophosphamide, and dexamethasone (p < 0.05). Disruption of the Hippo pathway attenuates the development of cALL by promoting cell proliferation, while suppressing apoptosis and drug sensitivity.