ABHD5 (Abhydrolase Domain Containing 5)

Moreover, it correlates with immune infiltration and may be relevant to immunotherapy in these cancers. Furthermore, its correlation with tumor protein 53 (TP53), alpha/beta hydrolase domain containing 5 (ABHD5), and evolutionarily conserved signaling intermediate in toll pathway (ECSIT) may be used as a potential area of therapeutic intervention.

Furthermore, ABHD5 overexpression continued to suppress c-MYC in PNPLA2-deficient cells, confirming a lipase-independent mechanism. These findings define a previously unrecognized role for ABHD5 as a negative regulator of c-MYC and highlight a novel, noncanonical pathway linking lipid metabolism regulators to oncogene control in prostate cancer.

Conversely, knocking down CGI-58 or PNPLA2 mimics I148M. We propose that I148M is a neomorph that exacerbates fatty liver risk by simultaneously impeding two major CGI-58-dependent pathways for liver triglyceride clearance: lipolysis and secretion.

In summary, our findings not only highlight PIGK as a novel molecular target in CRC but also suggest that targeting the PIGK-ABHD5-PPARα signaling axis could offer a promising therapeutic strategy. By influencing lipophagy, PIGK presents a potential avenue for improving CRC treatment outcomes, which could have significant implications for patient management and the development of new treatment protocols.

ABHD5 plays an important role in testicular tissue, and may be inseparable from testicular tumors and reproductive aging. However, its mechanism of action remains to be further studied.

Research has revealed a close association between ABHD5 and the development and progression of malignancies. This review summarizes the role of ABHD5 in various malignant tumors and explores the different signaling pathways and metabolic routes that may be involved, providing a comprehensive mechanistic understanding of ABHD5.

In general, our study demonstrates that FOXC1 exerts its tumor suppressor role by promoting ABHD5 transcription to regulating AMPK/mTOR signal pathway. FOXC1 could serve as both a diagnostic indicator and potential treatment focus for RCC.

MDSC express Bruton's Tyrosine Kinase (BTK) and BTK inhibition with ibrutinib, an FDA-approved irreversible inhibitor of BTK, leads to reduced MDSC expansion/function in mice and significantly improves the anti-tumor activity of anti-PD-1 antibody treatments...Pathway analysis revealed significantly downregulated pathways including TREM1, nitric oxide signaling, and IL 6 signaling (p<0.004). Implications: ScRNA-seq revealed characteristic gene expression patterns for MDSC from different cancer patients and BTK inhibition led to the downregulation of multiple genes and pathways important to MDSC function and migration.

The co-assembly hydrogel demonstrates good biocompatibility and enhanced gene transfection efficiency, efficiently triggering tumor cell apoptosis. Overall, the results of this study suggest that ABHD5 is a potential therapeutic target, and that a host-guest-based supramolecular hydrogel could serve as a promising platform for the inhibition of HCC.