HIC1 (HIC ZBTB Transcriptional Repressor 1)

A focused CD44 subnetwork further highlights ZNF521 (0.86) and HIC1 (0.65) as candidate regulators. These findings demonstrate that CTAS transforms cross-sectional data into dynamic regulatory insights and yields experimentally testable TFs that control AS during EMT.

Consistently, their depletion in human T cells reduces the expression of inhibitory receptors and improves effector function. By decoupling exhaustion TEX-selective from protective TRM cell programmes, our platform enables more precise engineering of T cell states, accelerating the rational design of more effective cellular immunotherapies.

Simultaneously targeting Prrx2 and Hic1 in macrophages significantly alleviated SU5416/hypoxia-induced PH in rats. The differential roles of pulmonary resMФs and recMФs in pulmonary vascular remodeling highlight novel therapeutic targets for pulmonary arterial hypertension treatment, specifically through inhibition of Hic1 and Prrx2 in macrophages.

Adult and embryonic MSCs exhibited overlapping H2AK119ub and H3K4me3/H3K27me3 (bivalent) histone marks, while SS18::SSX-mediated transformation culminated in the widespread loss of H3K27me3 at these genes and their consequent transcription. Collectively, these studies define a rare MSC context, conducive for SS18::SSX-mediated transformation, and demonstrate that SyS tumorigenesis involves the induction and maintenance of an embryonic-like MSC phenotype.

FBXW11 promotes the progression of AP by enhancing IRF1 transcription through the ubiquitination-mediated degradation of HIC1. Inhibition of FBXW11 or HIC1 effectively reduces the production of inflammatory cytokines and decreases cell apoptosis, thereby alleviating the symptoms of AP.

Conversely, AR and IRS2 inhibitors like EPI-7170 and NT157 negatively affected PCa progression. These results underscore HIC1's potential as a therapeutic target in PCa, offering new insights into its role in cancer biology and treatment.

© 2025 The Author(s). The Journal of Pathology published by John Wiley & Sons Ltd on behalf of The Pathological Society of Great Britain and Ireland

HSC-specific inhibition of HIC1 counteracted PP7-induced collagen depletion and HSC ferroptosis in vivo. These findings suggest that PP7 induces HSC ferroptosis through the HIC1/CX3CL1/GPX4 axis.

Characterized by the uvula muscle, the spatiotemporal dynamic process of soft palatal musculature of miniature pigs was revealed. Miniature pigs exhibit a similar structure of the uvula muscle to that of humans and therefore serve as a promising model for researching soft palatal musculature development of large mammals in the future.

Our results indicate that HIC1 genetic variants located in the zinc finger region affected its transcriptional repressor role. We can conclude that HIC1 may be involved in germline predisposition to SPS through an alteration of its repressor capacity and a faulty DNA damage response, as a molecular mechanism.

Integrated transcriptomic analysis indicated that HIC1 might regulate VSMC phenotypic modulation by activating Jag1 (Jagged 1) transcription. Our data suggest that Suv39h1 is a novel regulator of vascular injury and targeted for intervention of restenosis.

Additionally, c-Jun activation domain-binding protein 1 (Jab1) mediates the ubiquitylation and proteasomal degradation of HIC1 at Lys517. Ultimately, these findings underscore the potential of HIC1 as a promising immunotherapeutic target for the treatment of GC.