Altogether, these results describe the loss of CDO1 as a marker of aggressiveness in PCa. Furthermore, the loss of CDO1 is thought to be responsible for tumor progression in vitro by acting on multiple signaling pathways.
RNF214 promotes prostate tumor progression by ubiquitinating and targeting CAV1 for degradation, thereby sustaining mTOR signaling. These findings highlight the RNF214-CAV1 axis as a potential therapeutic target in PCa.
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PTEN (Phosphatase and tensin homolog) • CAV1 (Caveolin 1) • EIF4EBP1 (Eukaryotic translation initiation factor 4E binding protein 1)
In conclusion, our results revealed that DMAS induced activation of caspase cascades to elicit cell apoptosis in PC, through HO-1 upregulation and ERK/p38 activation. These findings provide possible avenues for the use of a naturally occurring compound with therapeutic values in fighting prostate carcinogenesis.
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HMOX1 (Heme Oxygenase 1) • XIAP (X-Linked Inhibitor Of Apoptosis)
EZH2 and PI3K pathway inhibitors achieve this by respectively inhibiting two key regulators of metabolism, MYC and HIF-1A, while concomitantly derepressing a pro-apoptotic stress sensor. Together, these studies reveal a promising therapeutic strategy for CRPC and demonstrate how metabolic plasticity can be fatally impaired by co-targeting upstream oncogenic nodes that converge on this important process.
P2, N=70, Active, not recruiting, University of Southern California | N=103 --> 70 | Trial completion date: Nov 2026 --> Dec 2030 | Trial primary completion date: Nov 2025 --> Dec 2027
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Enrollment change • Trial completion date • Trial primary completion date
P=N/A, N=800, Not yet recruiting, University of Michigan Rogel Cancer Center | Trial completion date: Nov 2029 --> Mar 2030 | Initiation date: May 2026 --> Sep 2026 | Trial primary completion date: Nov 2029 --> Mar 2030
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Trial completion date • Trial initiation date • Trial primary completion date