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Regulation of nuclear pre-mRNA domain-containing protein 1B (CREPT) is a transcriptional co-factor that is significantly overexpressed in a wide range of human malignancies [1, 2]. It plays a critical role in driving the cell cycle by interacting with RNA polymerase II and facilitating the formation of chromatin loops at the promoters of key oncogenes, such as Cyclin D1 and Cyclin B1 [4, 11]. This activity promotes the G1/S and G2/M transitions, leading to accelerated cell proliferation and tumor progression [1, 14]. Additionally, CREPT serves as a co-activator for several major signaling pathways, including Wnt/beta-catenin, STAT3, and NF-kappaB, further enhancing its oncogenic potential [2, 7, 10]. High levels of CREPT are strongly associated with poor clinical outcomes and reduced survival in patients with pancreatic, colorectal, and lung cancers [5, 9]. While there are currently no small-molecule inhibitors in clinical use, experimental strategies such as peptide-based PROTACs and gene therapy targeting the CREPT promoter have demonstrated efficacy in preclinical studies [11, 12]. CREPT also functions as a predictive biomarker, as its expression levels can influence the sensitivity of cancer cells to various chemotherapeutic agents [1, 2].
Targeted protein degradation, transcriptional repression, and RNA interference
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