ARHGAP5 (Rho GTPase Activating Protein 5)

In conclusion, our study elucidated new molecular mechanisms of nano-curcumin in the regulation of lncRNA expression and the discovery of potential targets in therapeutic interventions for CRC. More studies are needed to confirm the therapeutic implications of these findings.

These cells exhibited high-frequency mRNA splicing and exhibited specific crosstalk with T cells, distinguishing them from the subpopulation with the ARHGAP5 wild-type phenotype. Overall, this method provides a robust scRNA-seq platform suitable for comprehensive analyses of clinical specimens at different genetic information levels, thereby offering significant potential in the discovery of novel genes and interactions at the single-cell level.

This study provides a new approach to AML prognostic assessment and reveals the role of key genes in AML. These genes may become new biomarkers and therapeutic targets that can help improve prognostic prediction and personalized treatment of AML.

Notably, high-risk patients demonstrated higher sensitivity to Sorafenib, Oxaliplatin and MK-2206, underscoring the promise of these lncRNAs as precise therapeutic targets in bladder cancer. By revealing the predictive importance of disulfidptosis-associated lncRNAs in bladder cancer, our research offers new perspectives and pinpoints potential therapeutic targets in clinical environments.

These findings present potential actionable genomic markers of vincristine neuropathy and offer opportunities for tailored interventions to improve vincristine safety in children with cancer. This study is registered with ClinicalTrials.gov under the title National Active Surveillance Network and Pharmacogenomics of Adverse Drug Reactions in Children (ID NCT00414115, registered on December 21, 2006).

Further, we found that ARHGAP5 promotes epithelial-mesenchymal transition (EMT) by regulating Rho GTPases activities, and that ZFHX2-AS1 inhibits EMT in OCa by downregulating ARHGAP5 expression and suppressing the Rho GTPase signaling pathway. Taken together, our findings identify ZFHX2-AS1 as a potent tumor suppressor in OCa, acting through the modulation of DKC1-mediated pseudouridylation of ARHGAP5 and the inhibition of the Rho GTPase pathway, thus offering a potential therapeutic target for combating OCa progression.

Multivariate Cox regression proved ARHGAP5, ARHGAP11A, and ARHGAP12 could serve as independent prognostic indicators for PAAD. Finally, this study verified ARHGAP5, ARHGAP11A, and ARHGAP12 as independent prognostic factors in PAAD, suggesting their significance for the diagnosis and treatment of PAAD.

All compounds were tested for their inhibitory activity on MCF-7 cell growth, and compound 12 exhibited certain inhibitory effects on the growth of MCF-7 cells after 24 h of treatment at a concentration of 20 μM, with inhibition rates of 31.28%. Through target screening and molecular docking, human Rho GTPase activating protein 5 variant and human arachidonate 12-lipoxygenase (12S-type) might be important targets for compound 12 to exert anti-tumor activity.

Finally, we functionally validate that Arhgap5 and Mecom are tumor suppressor genes, providing possible therapeutic targets for CRC. Thus, we demonstrate the importance of the inactivation of senescence pathways in CRC development and progression in an inflammatory microenvironment, which can help progress toward precision medicine.

Finally, there was a significant positive association between tumor size and Knosp classification (χ = 11.5, p value = 0.02) and invasiveness of NFPA (χ = 6.12, p value = 0.04). The current study provides information about dysregulation of lncRNAs in NFPAs and warrants additional studies in this field.

Finally, quantitative RT-PCR showed that AC005261.1, AC021321.1, AL024508.2, LINC02446 and LINC01106 were lowly expressed in tumor cells, while ARHGAP5-AS1 showed the opposite trend. In summary, the predictive signature can independently predict the prognosis and provide clinical treatment guidance for BLCA patients.

Moreover, mutations with potential roles in immune evasion were identified. Overall, these data provide comprehensive insights into the molecular landscape of gastric cancer across various subtypes and ancestries.