PRKCB (Protein Kinase C Beta)

In conclusion, promoting DCN-mediated ferroptosis might be a potential strategy for enhancing the sensitivity of enzalutamide in PCa cells. This study delineates a novel mechanism by which DCN downregulation suppresses ferroptosis and drives enzalutamide resistance in CRPC.

PRKCB and SRD5A2 were identified as potential immunological biomarkers and immunotherapeutic targets associated with immune cell infiltration in PCa, both of which were significantly downregulated in PCa tissues. Moreover, kaempferol, isorhamnetin, and rhamnazin exhibited potential immunomodulatory effects in PCa by regulating the expression of PRKCB and SRD5A2.

Our findings elucidate multiple mechanisms by which CGs may exert anti-LSC activity, which could be crucial for the design of novel therapeutic strategies for AML. The proposed in silico framework is broadly applicable and may accelerate drug repurposing in AML and other cancers.

Immunoassays revealed that high-risk patients had 9 elevated immune checkpoints, while low-risk patients were more susceptible to pazopanib and temsirolimus. Real-time PCR (RT-qPCR) confirmed low levels of CASP7, PRKCB, and ENDOG mRNA in CRC tissues, with no significant difference between LMNB2 and GZMB. These findings highlight 5 MPTDN-associated prognostic genes in CRC, providing insights for individualized treatment and prognosis.

Rescue experiments were performed with the MAPK inhibitor trametinib...We reveal a novel oncogenic axis in which MYBL2 and SUMOylation cooperatively increase UBE2C expression and stability, promoting HCC progression via MAPK pathway activation. Targeting the MYBL2/UBE2C/MAPK axis represents a potential therapeutic strategy for treating HCC.

Wavelet-based individualized brain structural networks have been proposed for glioma grading models, resulting in novel imaging and molecular markers for cancer neuroscience.

Notably, elevated PKCβ levels enhance the efficacy of ferroptosis-inducing cancer therapies, while inhibition of the Ca2 +-PKCβ signaling pathway protects against acute pancreatitis by suppressing ferroptosis. These findings underscore the therapeutic potential of targeting Ca2 +-PKCβ-mediated ferroptosis, offering new avenues for the treatment of cancer and acute pancreatitis.

This study systematically characterizes the molecular landscape and features of primary breast tumors and their matched metastatic lymph nodes. These insights enhance our understanding of early-stage breast cancer metastasis and may pave the way for improved diagnostic tools and targeted therapeutic strategies.

By inhibiting PKCβ, MS-553 blocks B-cell receptor signaling and WNT/β-catenin and NF-κB functions, thereby inducing apoptosis in BTK inhibitor-resistant cells. See related article by Gordon et al., p. XX .

(Z)-endoxifen (hereafter endoxifen), the most abundant active tamoxifen metabolite, has emerged as a promising drug candidate due to its superior anti-estrogenic activity and favorable side effect profile...Resistant cells were characterized by stronger inhibition of the estrogen response, partial retention of endoxifen's antiproliferative effects, acquired activation of proinflammatory pathways and epithelial-mesenchymal transition (EMT), activation of the mTOR pathway (contrasting with its inhibition in sensitive cells), and elevated levels of PKCβ. These resistance-specific changes may potentially drive an endoxifen resistance phenotype and, therefore, proteins involved in these pathways may be proposed as potential therapeutic targets for overcoming endoxifen resistance in breast cancer.

These results suggest that the miR-4664-3p/PRKCB axis is crucial in NSCLC progression and immune modulation. Hence, MiR-4664-3p is a potential diagnostic and prognostic indicator, as well as therapeutic target in immunotherapy strategies for NSCLC.