ArticleMolecular cancer research : MCR2019
E-Cadherin Represses Anchorage-Independent Growth in Sarcomas through Both Signaling and Mechanical Mechanisms.
Article in Molecular cancer research : MCR, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 44 citations in OpenAlex.
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- Pediatric cancer-pathology and microenvironment influence: a perspective into osteosarcoma and non-osteogenic mesenchymal malignant neoplasms.Discover oncology · 2024Review
- Dual role of CASP8AP2/FLASH in regulating epithelial-to-mesenchymal transition plasticity (EMP).Translational oncology · 2024Article
- The functional role of Nudt2 in human triple negative breast cancer.Frontiers in oncology · 2024Article
- Dynamics and functions of E-cadherin complexes in epithelial cell and tissue morphogenesis.Marine life science & technology · 2023Review
- Genetic and Functional Modifications Associated with Ovarian Cancer Cell Aggregation and Limited Culture Conditions.International journal of molecular sciences · 2023Article
- Comparative Shotgun Proteomics Reveals the Characteristic Protein Signature of Osteosarcoma Subtypes.Cells · 2023Article
- Role of Nudt2 in Anchorage-Independent Growth and Cell Migration of Human Melanoma.International journal of molecular sciences · 2023Article
- Ewing sarcoma from molecular biology to the clinic.Frontiers in cell and developmental biology · 2023Review
- Predicting the immune microenvironment and prognosis with a anoikis - related signature in breast cancer.Frontiers in oncology · 2023Article
- Novel Targeted Therapeutic Strategies for Ewing Sarcoma.Cancers · 2022Review
- Semaphorin 3F induces colorectal cancer cell chemosensitivity by promoting P27 nuclear export.Frontiers in oncology · 2022Article
- Mapping phenotypic heterogeneity in melanoma onto the epithelial-hybrid-mesenchymal axis.Frontiers in oncology · 2022Article
- Tumor and Peripheral Immune Status in Soft Tissue Sarcoma: Implications for Immunotherapy.Cancers · 2021Review
- Curcumol inhibits the viability and invasion of colorectal cancer cells via miR-30a-5p and Hippo signaling pathway.Oncology letters · 2021Article
- VSP‑17 suppresses the migration and invasion of triple‑negative breast cancer cells through inhibition of the EMT process via the PPARγ/AMPK signaling pathway.Oncology reports · 2021Article
- Multi-Stability and Consequent Phenotypic Plasticity in AMPK-Akt Double Negative Feedback Loop in Cancer Cells.Journal of clinical medicine · 2021Article
- The Role of Noncoding RNAs in the Regulation of Anoikis and Anchorage-Independent Growth in Cancer.International journal of molecular sciences · 2021Review
- Review
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Authors and funding
23 authors at 6 institutions in 1 country.
Funding
Abstract
CDH1 (also known as E-cadherin), an epithelial-specific cell-cell adhesion molecule, plays multiple roles in maintaining adherens junctions, regulating migration and invasion, and mediating intracellular signaling. Downregulation of E-cadherin is a hallmark of epithelial-to-mesenchymal transition (EMT) and correlates with poor prognosis in multiple carcinomas. Conversely, upregulation of E-cadherin is prognostic for improved survival in sarcomas. Yet, despite the prognostic benefit of E-cadherin expression in sarcoma, the mechanistic significance of E-cadherin in sarcomas remains poorly understood. Here, by combining mathematical models with wet-bench experiments, we identify the core regulatory networks mediated by E-cadherin in sarcomas, and decipher their functional consequences. Unlike carcinomas, E-cadherin overexpression in sarcomas does not induce a mesenchymal-to-epithelial transition (MET). However, E-cadherin acts to reduce both anchorage-independent growth and spheroid formation of sarcoma cells. Ectopic E-cadherin expression acts to downregulate phosphorylated CREB1 (p-CREB) and the transcription factor, TBX2, to inhibit anchorage-independent growth. RNAi-mediated knockdown of TBX2 phenocopies the effect of E-cadherin on CREB levels and restores sensitivity to anchorage-independent growth in sarcoma cells. Beyond its signaling role, E-cadherin expression in sarcoma cells can also strengthen cell-cell adhesion and restricts spheroid growth through mechanical action. Together, our results demonstrate that E-cadherin inhibits sarcoma aggressiveness by preventing anchorage-independent growth. IMPLICATIONS: We highlight how E-cadherin can restrict aggressive behavior in sarcomas through both biochemical signaling and biomechanical effects.
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Registered trials
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