ArticleProceedings of the National Academy of Sciences of the United States of America2022
Superenhancer drives a tumor-specific splicing variant of MARCO to promote triple-negative breast cancer progression.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 23 papers, 2 of them syntheses that pooled it.
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Who cites it
23 citing papers in PubMed, 2 syntheses or guidelines pooled it, 31 citations in OpenAlex.
- Pooled it
- Application and prospect of organoid technology in breast cancer.Frontiers in immunology · 2024Pooled it
- Transcription Factor MAX Regulates Liver Cancer Cell Growth, Migration, Invasion, and Epithelial-Mesenchymal Transition by Promoting SF3A3 Expression.World journal of oncology · 2026Article
- Harnessing Tumor-Specific Transcript Diversity Uncovers a Shared Neoantigen Reservoir for Pancreatic Ductal Adenocarcinoma.MedComm · 2026Article
- Decoding neoantigen-encoding tumor-specific transcripts unveils a shared target reservoir for immunotherapy in hepatocellular carcinoma.Journal for immunotherapy of cancer · 2026Article
- Alternative splicing rewires breast cancer and opens therapeutic avenues.Cell communication and signaling : CCS · 2026Review
- Identification of altered immune landscape at single-cell resolution in NSCLC brain metastasis and its association with poor immune checkpoint inhibitor responses.Nature communications · 2026Article
- Establishment of Breast Cancer Organoids: A Systematic Review and Meta-Analysis.International journal of breast cancer · 2026Article
- Alternative Promoters Drive Transcriptomic Reprogramming and Prognostic Stratification in TNBC.NPJ systems biology and applications · 2025Article
- The SP1-SuperEnhancer-SPHK1 Axis Mediates Niraparib Resistance in TNBC.Pharmaceuticals (Basel, Switzerland) · 2025Article
- MARCO expression on myeloid-derived suppressor cells is essential for their differentiation and immunosuppression.Cell death discovery · 2025Article
- PLOD2 exacerbates cervical squamous cell carcinoma by suppressing p53 by binding to YAP1.Molecular medicine reports · 2025Article
- Current progress and future perspective of super-enhancers: a viable and effective bridge between the transcriptional apparatus and disease.Frontiers in genetics · 2025Review
- Targeting SNRNP200-induced splicing dysregulation offers an immunotherapy opportunity for glycolytic triple-negative breast cancer.Cell discovery · 2024Article
- Mechanisms of RNA alternative splicing dysregulation in triple-negative breast cancer.Zhong nan da xue xue bao. Yi xue ban = Journal of Central South University. Medical sciences · 2024Review
- Integrated genomic and transcriptomic analysis reveals the activation of PI3K signaling pathway in HPV-independent cervical cancers.British journal of cancer · 2024Article
- The application of MARCO for immune regulation and treatment.Molecular biology reports · 2024Review
- Natural plant-derived polysaccharides targeting macrophage polarization: a promising strategy for cancer immunotherapy.Frontiers in immunology · 2024Review
- KLHL29-mediated DDX3X degradation promotes chemosensitivity by abrogating cell cycle checkpoint in triple-negative breast cancer.Oncogene · 2023Article
- KLF5 Promotes Tumor Progression and Parp Inhibitor Resistance in Ovarian Cancer.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The transcription variation, leading to various forms of transcripts and protein diversity, remains largely unexplored in triple-negative breast cancers (TNBCs). Here, we presented a comprehensive analysis of RNA splicing in breast cancer to illustrate the biological function and clinical implications of tumor-specific transcripts (TSTs) arising from these splicing junctions. Aberrant RNA splicing or TSTs were frequently harbored in TNBC and were correlated with a poor outcome. We discovered a tumor-specific splicing variant of macrophage receptor with collagenous structure-TST (MARCO-TST), which was distinguished from myeloid cell-specific wild-type MARCO. MARCO-TST expression was associated with poor outcomes in TNBC patients and could promote tumor progression in vitro and in vivo. Mechanically, MARCO-TST interacted with PLOD2 and enhanced the stability of HIF-1α, which resulted in the metabolic dysregulation of TNBC to form a hypoxic tumor microenvironment. MARCO-TST was initiated from a de novo alternative transcription initiation site that was activated by a superenhancer. Tumors with MARCO-TST expression conferred greater sensitivity to bromodomain and extraterminal protein inhibitors. This treatment strategy was further validated in patient-derived organoids. In conclusion, our results revealed the transcription variation landscape of TNBC, highlighting MARCO-TST as a crucial oncogenic transcript and therapeutic target.
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