HEXIM1 (HEXIM P-TEFb Complex Subunit 1)

In contrast, HEXIM1+CAF-C1 may act as an independent risk factor for poor prognosis in CRC. Our findings enhance understanding of immune escape mechanisms in CRC, show how novel subtypes affect prognosis, and offer insights for new diagnostic and treatment strategies.

The consistent downregulation of GATA1, NFE2, and PF4 transcription within hours post-BMS-986158 treatment in both preclinical and clinical studies demonstrates that BET inhibitors induce thrombocytopenia by altering GATA1 gene expression and its downstream genes, NFE2 and PF4, which regulate megakaryopoiesis and thrombopoiesis. Early detection of transcriptional changes in blood samples during treatment courses positions NFE2 and PF4 as promising biomarkers for proactively monitoring and mitigating treatment-emergent thrombocytopenia.

Finally, we show that tRNA splicing machinery is involved with the formation of some MHV68-induced tRFs, with a key regulator of splicing, CLP1, required for maximal viral titer. Taken together, we posit that tRNA processing may be integral to the elegant shift in gene expression that occurs during viral takeover of the host cell.

Emerging evidence implicates 7SK snRNP deregulation in cancer progression. This review explores the intricate interplay between 7SK snRNP and CDK9, highlighting how disruptions in individual 7SK snRNP components drive transcriptional imbalances, amplify oncogenic programs, and promote a tumorigenic environment.

We observed the augmentation of DNA damage response to Doxorubicin in the presence of KDM5Bi, and this action is a contributing factor in KDM5Bi-induced IFN-I...Via the upregulation of HEXIM1, KDM5Bi represent pharmacologically induced and tumor intrinsic IFN-I production that is cGAS/STING independent. This is critical because cGAS/STING induce an inflammatory response that promotes the survival of cancer cells, and STING is often impaired in malignant cancers.

We conclude that the tumor suppressors DAF-18/PTEN and LIN-35/Rb function in a linear pathway, with LIN-35/Rb and the rest of the DREAM complex functioning as a transcriptional effector of DAF-18/PTEN protein-phosphatase activity resulting in repression of germline gene expression. This work is significant for revealing a network of tumor suppressors that promote survival during cellular and developmental quiescence.

PDO-based NAC shows a promising resectable rate in BRPC patients, with good tolerance. Potential drug-resistant and sensitive genes and cell-cell interaction changes may participate in the development of gemcitabine resistance.

We conclude that the tumor suppressors DAF-18/PTEN and LIN-35/Rb function in a linear pathway, with LIN-35/Rb and the rest of the DREAM complex functioning as a transcriptional effector of DAF-18/PTEN protein-phosphatase activity resulting in repression of germline gene expression. This work is significant for revealing a network of tumor suppressors that promote survival during cellular and developmental quiescence.

At the same time, HEXIM1 knockdown reversed the antitumor effects of USP44. These findings demonstrated that USP44 acted as a critical tumor suppressor in OSCC by inhibiting cell proliferation and metastasis through the stabilization of HEXIM1 protein, suggesting that USP44-HEXIM1 axis is a promising target for OSCC therapy.

The expression of PLEC was strongly correlated with the sensitivity of gefitinib, a classical EGFR inhibitor. R-loop binding proteins have been identified as significant determinants in the prognosis and therapeutic strategies for lung adenocarcinoma. The results indicates that therapeutic interventions targeting these specific R-loop binding proteins might contribute to a better survival in lung cancer patients.

It raises intriguing questions about whether other herpesviruses employ similar mechanisms to manipulate HEXIM1 and if this molecular target can be exploited to limit productive replication. Thus, this discovery not only contributes to our understanding of herpesvirus infection regulation but also holds implications for broader research on other herpesviruses, even DNA viruses.

P1, N=60, Recruiting, National Cancer Institute (NCI) | Initiation date: May 2024 --> Dec 2023