ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2024
Super-Enhancer Reprograming Driven by SOX9 and TCF7L2 Represents Transcription-Targeted Therapeutic Vulnerability for Treating Gallbladder Cancer.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Identification and characterization of POSTNJournal of orthopaedic translation · 2026Article
- Super-enhancer-driven ITGB2-AS1 promotes ovarian cancer progression by binding to IQGAP1.Translational oncology · 2026Article
- Oncogenic GPRIN1 sustains proliferation and mitochondrial homeostasis via dual‑layer CDK1-PI3K/Akt signalling in gallbladder cancer.Cell death & disease · 2026Article
- Macrophage-rich niches regulate T cell dynamics at the liver invasive margin during gallbladder cancer progression.The Journal of clinical investigation · 2026Article
- Sex-Related Differences in Histone Acetylation and Tumor Development in a 4-Nitroquinoline 1-Oxide and Ethanol-Induced Oral Squamous Cell Carcinoma Mouse Model.Journal of oral pathology & medicine : official publication of the International Association of Oral Pathologists and the American Academy of Oral Pathology · 2025Article
- Enhancer reprogramming: critical roles in cancer and promising therapeutic strategies.Cell death discovery · 2025Review
- Lactylation in digestive system tumors: from mechanisms to therapeutic target.Frontiers in oncology · 2025Review
- Super-Enhancer Reprograming Driven by SOX9 and TCF7L2 Represents Transcription-Targeted Therapeutic Vulnerability for Treating Gallbladder Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
Corrections and comments
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Authors and funding
23 authors.
Funding
Abstract
Gallbladder cancer (GBC) is a highly aggressive malignancy lacking clinically available targeted therapeutic agents. Super-enhancers (SEs) are crucial epigenetic cis-regulatory elements whose extensive reprogramming drives aberrant transcription in cancers. To study SE in GBC, the genomic distribution of H3K27ac is profiled in multiple GBC tissue and cell line samples to establish the SE landscape and its associated core regulatory circuitry (CRC). The biliary lineage factor SOX9 and Wnt pathway effector TCF7L2, two master transcription factor (TF) candidates identified by CRC analysis, are verified to co-occupy each other's SE region, forming a mutually autoregulatory loop to drive oncogenic SE reprogramming in a subset of GBC. The SOX9/TCF7L2 double-high GBC cells are highly dependent on the two TFs and enriched of SE-associated gene signatures related to stemness, ErbB and Wnt pathways. Patients with more such GBC cells exhibited significantly worse prognosis. Furthermore, SOX9/TCF7L2 double-high GBC preclinical models are found to be susceptible to SE-targeted CDK7 inhibition therapy in vitro and in vivo. Together, this study provides novel insights into the epigenetic mechanisms underlying the oncogenesis of a subset of GBCs with poorer prognosis and illustrates promising prognostic stratification and therapeutic strategies for treating those GBC patients in future clinical trials.
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