HDAC6 (Histone Deacetylase 6)

This study demonstrates LukS-PV targets C5aR to inhibit HCC EMT via the BCL6/HDAC6/HSPD1 axis, highlighting its potential as an HCC therapeutic agent. These findings provide valuable EMT regulatory insights and identify potential HCC therapeutic targets.

Treatment of PDOs led to a dose-dependent reduction in viability and clonogenic capacity, accompanied by downregulation of stemness and proliferation markers. Overall, these findings demonstrate that selective HDAC6 inhibition by Mesinostat modulates key oncogenic pathways in TNBC, supporting its potential as a promising therapeutic approach for HDAC6-overexpressing breast cancers.

Autophagy was triggered by upregulating LC3 and Atg-7 expression. Collectively, these findings suggest that BKS-112 exerts robust anticancer effects by inducing cell cycle arrest, apoptosis, and autophagy, highlighting its therapeutic promise for TNBC treatment.

These findings suggest LPXN may influence breast cancer progression through HDAC6/EGR2-mediated regulation of macrophage polarization. In conclusion, our study demonstrated that the LPXN/HDAC6/EGR2 axis promotes breast cancer progression by augmenting macrophage M2 polarization.

Moreover, pharmacological inhibition of HDAC with Trichostatin A (TSA) suppressed both HDAC6 and BNIP3 expression, decreased autophagic activity, and reduced lung tumor formation in a KRASG12D+/P53loxP/loxP transgenic mouse model. Collectively, these results reveal a novel HDAC6-HIF-1α-BNIP3 axis that governs autophagy in lung cancer and underscore the potential of HDAC6 as a therapeutic target for modulating autophagy and inhibiting lung tumor progression.

Notably, TALDO1 deacetylation inhibited its nuclear translocation and interaction with BRCA1, thereby reducing the inhibition of c-Myc transcriptional activation, promoting the expression of HK2/LDHA/PDK1, and further enhancing glycolysis independent of TALDO1 enzyme activity. This research elucidated the regulatory mechanism of TALDO1 from the perspective of acetylation modification, clarified the moonlighting functions of TALDO1 in metabolic reprogramming, and provided novel biomarkers and intervention strategies, such as HDAC inhibitors, for the clinical treatment of NPC.

Additionally, TSA enhanced T-cell-mediated anti-tumor immunity, as indicated by lower levels of CD8a+PD1+ and CD4+PD1+ regulatory T cells and higher levels of CD8a+Granzyme+, CD4+Granzyme+, CD8a+IFNγ+, and CD4+IFNγ+ cells in the spleen and tumor. In conclusion, TSA attenuates RIPK1/RIPK3/MLKL-signalling and reprograms the immunosuppressive TME, inhibiting OSCC progression and highlighting its potential as a therapeutic agent in clinical conditions.

The HDI-3 emerged as the most promising candidate among replicate simulations, exhibiting a substantially favorable MM/GBSA binding free energy of -130.67 kcal/mol-indicative of strong thermodynamic stability and stronger binding affinity compared to reference inhibitors Trichostatin A and Ricolinostat. Therefore, experimental validation is essential to confirm the compound's efficacy and safety. This integrated computational pipeline provides an efficient strategy to accelerate targeted drug discovery, laying the groundwork for future experimental investigations.

This new pathway suggests that in ALS the aggregation of TDP-43 leads to the overexpression of HDAC6 which impairs autophagy pathway. Thus, our work suggest that in sALS HDAC6 should be tuned and these findings could be exploited in the future as possible therapeutic target.

This review summarizes the functions of HDAC6, its roles in different disorders, and various types of modulators targeting HDAC6. These insights may provide valuable information for further design of therapeutic drugs by targeting HDAC6.

Mutual exclusivity was observed between PIK3CA exon 20 mutations and SNPs. The -124C>T TERT promoter mutation may serve as a favorable prognostic marker in OCCC, while p53 mutations and reduced HDAC6 expression are associated with poor outcomes.

Mechanistically, ZNF295-AS1 functions as a competing endogenous RNA, sponging miR-762 and thus relieving the repression of HDAC6, ultimately influencing autophagy and tumor progression. In conclusion, ZNF295-AS1 is implicated in the regulation of autophagy and malignancy in NPC through the miR-762/HDAC6 axis, suggesting its potential as a novel diagnostic and therapeutic target in NPC management.