HDAC6 expression

These data suggest that pharmacologically amenable kinase-independent functions of HDAC6 control viral replication. Eliminating HDAC6 could be a promising anti-viral strategy with a benign impact on host cells.

Finally, we examine the relationships among MAP3K4, TRAF4, and HDAC6 in the developing placenta, finding a previously unknown switch in coexpression of Traf4 with Map3k4 versus Traf4 with Hdac6 during differentiation of the placental labyrinth. Together, our findings identify previously unknown mechanisms of MAP3K4 and HDAC6 coregulation of TRAF4 in TS cells and highlight these MAP3K4, TRAF4, and HDAC6 associations during placental development.

Our findings encourage the exploration of the role of HDAC6 as a prognostic factor and the combinatorial use of HDAC6 selective inhibitors combined with trastuzumab in HER2+ BC, in particular for those patients experiencing drug resistance.

The upregulation of HDAC6 induced by METTL3 over-expression is capable of inhibiting cilia elongation and acetylation of α-tubulin, thereby shortening cilia length and accelerating the progression of cervical cancer both in vitro and in vivo. Collectively, depletion of METTL3-mediated m6A modification leads to abnormally elongated cilia via suppressing HDAC6-dependent deacetylation of axonemal α-tubulin, ultimately attenuating cell growth and cervical cancer development.

Additionally, HDAC6 and DNMT3B are emerging as important therapeutic targets for cancer. This study lays the foundation for further exploration of the oncogenic mechanisms of HPV E6/E7 and may provide new directions for the treatment of HPV-related cancers.

Notably, the addition of HDAC6 inhibitor potentiated the effects of anti-ER and anti-PR drugs mainly in TNBC cells. Together, these data highlight the role of HDAC6 in regulating PR expression and provide a promising therapeutic approach for boosting breast cancer sensitivity to hormonal therapy.

In conclusion, our results demonstrate a complex expression pattern of HDAC6 depending on ARID1A status in different endometriosis subtypes. Further studies on HDAC6 and ARID1A are important to elucidate mechanisms involved in malignant transformation of endometriosis.

A new prognostic model for OS, associated with LCD-RGs, was developed and validated, offering a fresh perspective for exploring the association between LCD and OS.

P=N/A, N=150, Not yet recruiting, Yale University

Nocodazole pre-treatment proved that TSA inhibited the lysosomal exocytosis of IL-1β through tubulin acetylation. In conclusion, HDAC6 inhibitors attenuated TME and cancer progression through the regulation of IL-1β in OSCC.

Importantly, MDH1 siRNA clearly reversed the protection of LT-630 on APAP-stimulated AML-12 cells. In conclusion, LT-630 could ameliorate liver injury by modulating MDH1-mediated oxidative stress induced by APAP.

The data suggest that 25202 is a novel selective and potent HDAC6 inhibitor. Compound 25202 blocks HDAC6 activity and interferes microtubule dynamics, leading to SAC activation and mitotic arrest prolongation that eventually cause apoptosis of CRPC cells. Furthermore, 25202 sensitizes cisplatin-induced cell apoptosis through impeding DNA damage repair pathways.