ArticleOncogene2022
Canonical TGFβ signaling induces collective invasion in colorectal carcinogenesis through a Snail1- and Zeb1-independent partial EMT.
Article in Oncogene, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed.
- Clusters, fingers, and singles: A mechanical landscape of tumor invasion.PLoS computational biology · 2026Article
- Comparative Transcriptomic Analysis of Oral Squamous Cell Carcinoma with Progressive Cisplatin Resistance.International journal of molecular sciences · 2026Article
- Deciphering the impact ofGenes & diseases · 2026Article
- Transcriptomic Signatures Associated with Doxorubicin Treatment in Liposarcoma Reveal Coordinated Regulatory Patterns.Diseases (Basel, Switzerland) · 2026Article
- Multidimensional dissection of shared genetic susceptibility in ulcerative colitis and colorectal cancer: novel insights from integrative single-cell and multi-omics analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Article
- Serum uric acid and its metabolism-a vital factor in the inflammatory transformation of cancer.Journal of advanced research · 2026Review
- Mechanisms Underlying the Initiation and Termination of Collective Cell Migration: Perspectives for Understanding Development and Cancer Metastasis.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026Review
- Emerging KRAS G12D inhibitor in the treatment of digestive system tumors: opportunities and challenges.Translational gastroenterology and hepatology · 2026Review
- Cytokine and chemokine networks in colorectal cancer.Frontiers in immunology · 2026Review
- Single-cell multiomic modelling of early metastatic events promoted by the extracellular matrix.British journal of cancer · 2025Article
- Partial-EMT cell state correlates with single cell pattern of invasion in head and neck SCC keratinocytes.The Journal of pathology · 2025Article
- The atypical KRASMolecular oncology · 2025Article
- TGF-β signaling redirects Sox11 gene regulatory activity to promote partial EMT and collective invasion of oncogenically transformed intestinal organoids.Oncogenesis · 2025Article
- Mechanisms of breast cancer metastasis: the role of extracellular matrix.Molecular and cellular biochemistry · 2025Review
- KRAS inhibitors may prevent colorectal cancer metachronous metastasis by suppressing TGF‑β mediated epithelial‑mesenchymal transition.Molecular medicine reports · 2025Article
- TGFβ in Pancreas and Colorectal Cancer: Opportunities to Overcome Therapeutic Resistance.Clinical cancer research : an official journal of the American Association for Cancer Research · 2024Review
- Let-7a-3p overexpression increases chemosensitivity to carmustine and synergistically promotes autophagy and suppresses cell survival in U87MG glioblastoma cancer cells.Naunyn-Schmiedeberg's archives of pharmacology · 2024Article
- Role of miRNA-mRNA Interactome in Pathophysiology of Arrhythmogenic Cardiomyopathy.Biomedicines · 2024Article
- The receptor protein tyrosine phosphatase PTPRK promotes intestinal repair and catalysis-independent tumour suppression.Journal of cell science · 2024Article
- Secretion of WNT7A by UC-MSCs assist in promoting the endometrial epithelial regeneration.iScience · 2024Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Local invasion is the initial step towards metastasis, the main cause of cancer mortality. In human colorectal cancer (CRC), malignant cells predominantly invade as cohesive collectives and may undergo partial epithelial-mesenchymal transition (pEMT) at the invasive front. How this particular mode of stromal infiltration is generated is unknown. Here we investigated the impact of oncogenic transformation and the microenvironment on tumor cell invasion using genetically engineered organoids as CRC models. We found that inactivation of the Apc tumor suppressor combined with expression of oncogenic Kras
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