Our study unveils the critical roles of palmitoylation-modifying enzymes in ccRCC progression and immune regulation. The identified key genes hold promise as biomarkers for diagnosis and prognosis, offering potential targets for future therapeutic strategies.
Collectively, ZDHHC11 regulates osimertinib resistance in a palmitoylation-dependent manner. Targeting the ZDHHC11-AXL axis may provide a promising therapeutic strategy for the treatment of osimertinib-resistant EGFR-mutant NSCLC patients with high ZDHHC11 expression.
Analysis on drug sensitivity revealed that the high-risk group was highly sensitive to rapamycin. Additionally, it was verified that IFFO1, ANKRD10 and POLG2 were markedly upregulated and CHMP4A was also markedly downregulated in A375 cells by RT-PCR, which was consistent with the partial results of biological analysis. Overall, it would provide valuable information about the GRGs of prognosis and immune status in melanoma.
This is the first study showing a critical role for palmitoylation in controlling growth of B-cell lymphoma. Moreover, we provide evidence that next to the previously identified ZDHHC11, ZDHHC18 is also crucial for B-cell lymphoma growth expanding the potential functional role for ZDHHC family members in lymphomagenesis.
Furthermore, we systemically reviewed the literatures on leukemia and DNA methylation modifications, providing a comprehensive description of their correlation. In summary, these findings indicate that DNA methylation plays a crucial role in the onset and progression of ALL, offering valuable insights for future research into its impact on leukemia development.
We first performed the comprehensive analysis of MPTDN in NSCLC and screened three NSCLC-related biomarkers as promising biomarkers. ARL14 might be a new potential target for therapy of NSCLC.
This indicated that the miR-150 binding site region is dispensable for the growth promoting role of circZDHHC11. To conclude, our results show that circZDHHC11 is a crucial factor supporting BL cell growth independent of its ability to sponge miR-150.
Our findings indicated that ZDHHC11B plays a significant role in inhibiting tumorigenesis via EMT. In addition, ZDHHC11B may be a candidate molecular target for LUAD treatment.