ArticleCell reports2020
Epigenomic Reprogramming toward Mesenchymal-Epithelial Transition in Ovarian-Cancer-Associated Mesenchymal Stem Cells Drives Metastasis.
Article in Cell reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
What it found
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Who cites it
49 citing papers in PubMed, 91 citations in OpenAlex.
- Epigenetic mechanisms and clinical translation in ovarian cancer: from molecular pathways to precision therapy.Bioscience reports · 2026Review
- Tertiary lymphoid structures in cancer: their development, composition, clinical prognosis, and the drivers of the anti-tumor responses.Molecular biomedicine · 2026Review
- Mesenchymal stromal/stem cells in tumour initiation, progression and therapy.Nature reviews. Cancer · 2026Review
- Rethinking ovarian cancer III: the past decade and future directions.Nature reviews. Cancer · 2026Review
- Mapping immunosuppressive terrain in high-grade serous ovarian cancer: tumor-intrinsic, stromal, and spatial drivers of therapy response.NPJ precision oncology · 2026Review
- Mesenchymal stem cell therapy for premature ovarian insufficiency: progress and challenges.Journal of ovarian research · 2026Review
- Orchestration of tertiary lymphoid structures: decoding developmental mechanisms for next-generation cancer immunotherapies.Medical review (2021) · 2025Article
- miR‑145 and miR‑23b co‑transfection decreases proliferation, migration, invasion and protein levels of c‑MYC, ZEB1 and ABCB1 in epithelial ovarian cancer cell lines.Molecular medicine reports · 2025Article
- Tumor-associated mesenchymal stem/stromal cells in tumor microenvironment and carcinogenesis.Experimental hematology & oncology · 2025Review
- High metastatic tumor-derived CXCL16 mediates liver colonization metastasis by inducing Kupffer cell polarization via the PI3K/AKT/FOXO3a pathway.Neoplasia (New York, N.Y.) · 2025Article
- Aged and BRCA-Mutated Stromal Cells Drive Epithelial Cell Transformation.Cancer discovery · 2025Article
- Past failures and new horizons: the nuances of tertiary lymphoid structures in high-grade serous ovarian cancer may contribute to immunotherapy effectiveness.Journal for immunotherapy of cancer · 2025Review
- APOBEC3A drives ovarian cancer metastasis by altering epithelial-mesenchymal transition.JCI insight · 2025Article
- Article
- Epigenetic dynamics in meniscus cell migration and its zonal dependency in response to inflammatory conditions.APL bioengineering · 2025Article
- Crosstalk between stromal, immune, and ovarian cancer cells in lipid-rich tumor microenvironment exhibits proliferative features.Frontiers in immunology · 2025Review
- Tertiary lymphoid structures: exploring opportunities to improve immunotherapy in ovarian cancer.Frontiers in immunology · 2025Review
- Unveiling the power of mitochondrial transfer in cancer progression: a perspective in ovarian cancer.Journal of ovarian research · 2024Review
- Loss of XIST lncRNA unlocks stemness and cellular plasticity in ovarian cancer.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- The activity of tertiary lymphoid structures in high grade serous ovarian cancer is governed by site, stroma, and cellular interactions.Cancer cell · 2024Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 1 country.
Funding
Abstract
A role for cancer cell epithelial-to-mesenchymal transition (EMT) in cancer is well established. Here, we show that, in addition to cancer cell EMT, ovarian cancer cell metastasis relies on an epigenomic mesenchymal-to-epithelial transition (MET) in host mesenchymal stem cells (MSCs). These reprogrammed MSCs, termed carcinoma-associated MSCs (CA-MSCs), acquire pro-tumorigenic functions and directly bind cancer cells to serve as a metastatic driver/chaperone. Cancer cells induce this epigenomic MET characterized by enhancer-enriched DNA hypermethylation, altered chromatin accessibility, and differential histone modifications. This phenomenon appears clinically relevant, as CA-MSC MET is highly correlated with patient survival. Mechanistically, mirroring MET observed in development, MET in CA-MSCs is mediated by WT1 and EZH2. Importantly, EZH2 inhibitors, which are clinically available, significantly inhibited CA-MSC-mediated metastasis in mouse models of ovarian cancer.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.