CTBP1 (C-Terminal Binding Protein 1)

The consistent alterations suggest the presence of a shared Notch-driven oncogenic signature in breast cancer, potentially driving cell proliferation, stemness, and resistance to therapy. These findings enhance our understanding of Notch signaling in breast cancer and propose novel miRNA-Notch interactions as candidate targets for therapeutic intervention.

In colorectal carcinoma (CRC) cells, CtBP2 and G9a co-occupy the PTEN promoter, where disruption of their interface reduces H3K9me2 deposition, derepresses PTEN expression, attenuates PI3K-AKT signaling, and impairs CRC cell proliferation. Together, these findings establish a structural framework for CtBP-mediated regulation of G9a activity and highlight the CtBP1/2-G9a complex as a potential therapeutic target in colorectal cancer.

The observational and exploratory components warrant validation in larger cohorts and functional assays. To our knowledge, this is the first integrative study combining GWAS, single-cell eQTL and MRI radiomics to prioritize CTBP1 in breast cancer.

Highlighting translational potential in late-stage HGSOC, combined JW-98/GMX1778 treatment of platinum-resistant OVCAR3 HGSOC mouse xenografts abrogated tumor growth without observable toxicity. Combined inhibition of CtBP and NAD synthesis represents a novel therapeutic strategy that could improve outcomes in chemoresistant HGSOC.

Our study reveals that SIRT5-mediated CTBP1 succinylation drives HCC progression through MAT1A suppression, establishing a novel regulatory axis with therapeutic potential for HCC treatment.

Our research indicates that FTY720 may inhibit NSCLC via possible targets ZEB2 and S1PR1, further laying the theoretical foundation for the utilization of FTY720 in NSCLC treatment.

The EWSR1::CTBP1 gene fusion has never previously been reported in uterine tumours, having been reported in the literature only once, in the context of a gastroblastoma. The presented case expands the range of the gene-fusion-associated mesenchymal tumours of the uterus.

Molecular docking analysis illustrated JQ1 may promote AXIN1 expression. This study is the first to identify AXIN1 as a replication stress associated gene with prognostic value in CC, specifically in the context of radiotherapy. These findings may support personalized treatment strategies and provide a foundation for future investigations into RS-targeted therapies in CC.

Our findings suggest that stemness-related heterogeneity in LMS shapes the tumor immune microenvironment and contributes to disease progression. The six identified prognostic markers not only provide insights into the molecular mechanisms of LMS but also represent potential therapeutic targets for personalized treatment.

Experimental validation with RT-qPCR confirmed the differential expression of the candidate biomarkers (ARRB1, RPS3A, COL4A5, COL1A2 and MED10) across the three CRC stages reinforcing their potential as stage-specific biomarkers in CRC progression. These findings provide a foundation to distinguish between the CRC stages and for the development of accurate stage-specific diagnostic and prognostic biomarkers, which helps in the development of more effective therapeutic strategies for CRC.

Importantly, it also encodes the microprotein DNA damage up-regulated protein (DDUP), which mediates cisplatin resistance through sustained response to DNA damage signals. Furthermore, CTBP1-DT has been implicated in the progression of non-malignant diseases such as diabetes and related conditions, cardiovascular diseases, and osteoarthritis. This review summarizes the latest research on the RNA and protein functions of CTBP1-DT in human diseases, outlines various molecular regulatory networks centered around CTBP1-DT, and discusses the opportunities and challenges of its clinical applications.