PRKCA (Protein Kinase C Alpha)

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.

Evidence for molecular and treatment-related factors is limited and requires further validation. These findings highlight the need for standardized reporting and prospective studies tailored to young-onset disease.

This study demonstrates that EB, a natural compound from E. lindleyanum, serves as a potent anti-fibrotic agent by directly targeting PKCα and inhibiting the PKCα/AKT/mTOR axis. These findings provide a novel therapeutic lead for liver fibrosis and offer scientific validation for the traditional use of E. lindleyanum in treating inflammation-related disorders, highlighting the value of exploring traditional herbal constituents for modern molecular targets.

Six compounds were isolated from H. giganteus, with 4 exhibiting antiproliferative activity through PRKCA and GSK3β modulation. These findings provide the first phytochemical and mechanistic evidence that support H. giganteus as a promising source of active anti-colon cancer leads.

This process attenuates p38 MAPK phosphorylation, which in turn drives BC progression. Together, our work defines a key signaling axis-DTX3L-PKCα-p38 MAPK-in BC progression and provide important insights for the diagnosis and treatment of this disease.

FTA treatment promoted Beclin-1 and LC3B II/LC3B I expressions, and inhibited PKCα and p-p65/p65 expressions in prostate tissues of CNP rat models. FTA alleviates inflammation and facilitates autophagy in CNP rat models by blocking the PKCα/NF-κB pathway.

The overexpression of ATP synthase-related proteins ATP5A1 and ATP5C1 in the tumor microenvironment of MDA-MB-231 xenograft mice were also significantly suppressed by DET and DETD-35 treatments. In summary, this study identifies DETD-35 and DET as novel ATPase inhibitors which are attributed to disrupting mitochondrial biogenetics and cellular metabolism and networking in TNBC cells.

In vitro 2D cytotoxicity assays demonstrated potent antiproliferative activity, with IC₅₀ values of 3.93 ± 0.47 μM in A549 and 4.88 ± 1.42 μM in non-small cell lung cancer (NSCLC) cells, while showing reduced cytotoxicity in normal fibroblasts (MRC-5; IC₅₀ = 10.48 ± 1.83 μM) compared with osimertinib. Molecular docking and in silico conformational analyses demonstrated strong binding affinity of compound 3 to the VEGFR-2 kinase domain, stabilizing critical active-site residues and supporting a structure-based mechanism of action. Collectively, these findings validate VEGFR-2 as a therapeutic target and highlight compound 3 as a promising scaffold for structure-based drug development against non-small cell lung cancer.

Gastric cancer (GC) is often associated with high invasiveness, epithelial-mesenchymal transition (EMT), and resistance to 5-fluorouracil (5-FU), highlighting the need for novel therapeutic targets...DADS inhibits GC progression and enhances 5-FU sensitivity by PKCα/RORα-mediated downregulation of RORα/β-catenin signaling, paralleling SR1078/TPA effects. It may act as a novel RORα agonist for GC therapy.

Current chemotherapy treatments, including the TIP (Taxol, Ifosfamide, Cisplatin) regimen, have shown limited effects but strong side effects in advanced Penile squamous cell carcinoma (PSCC) patients. Furthermore, compared with cisplatin, TROP-2 targeted ADC could achieve an equivalent inhibitory effect on the proliferation of PSCC both in vivo and in vitro. TROP-2 promoted PSCC cell proliferation via AKT/PKCα-dependent pathway, and TROP-2-targeted ADC-drug has a gratifying inhibitory effect on PSCC proliferation both in vivo and in vitro.

Unexpectedly, increased editing levels in select genes ( CD247 , PRKCA and TRAF3IP2.ASI in T-ALL; SPPL3 in B-ALL) were significantly associated with better patient survival, suggesting a potential prognostic role for editing dysregulation at individual gene levels. Together, these results deepen our understanding of the pediatric ALL transcriptome landscape and provided novel candidate regulators and therapeutic targets for future mechanistic and translational investigation.