ArticleProtein & cell2021
Loss of 4.1N in epithelial ovarian cancer results in EMT and matrix-detached cell death resistance.
Article in Protein & cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 24 citations in OpenAlex.
- Unraveling the anoikis-cancer nexus: a bibliometric analysis of research trends and mechanisms.Future science OA · 2025Article
- Processed Products ofAnti-cancer agents in medicinal chemistry · 2025Article
- Cell hiding in colorectal cancer: correlation with response to chemotherapy in vitro and in vivo.Scientific reports · 2024Article
- Restoring BARX2 in OSCC reverses partial EMT and suppresses metastasis through miR-186-5p/miR-378a-3p-dependent SERPINE2 inhibition.Oncogene · 2024Article
- Entosis: the core mechanism and crosstalk with other cell death programs.Experimental & molecular medicine · 2024Article
- Mechanisms and significance of entosis for tumour growth and progression.Cell death discovery · 2024Review
- mTORC1 Mediates Biphasic Mechano-Response to Orchestrate Adhesion-Dependent Cell Growth and Anoikis Resistance.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- Nuclear isoform of RAPH1 interacts with FOXQ1 to promote aggressiveness and radioresistance in breast cancer.Cell death & disease · 2023Article
- Defining the Role of Metastasis-Initiating Cells in Promoting Carcinogenesis in Ovarian Cancer.Biology · 2023Review
- The crosstalk between anoikis and epithelial-mesenchymal transition and their synergistic roles in predicting prognosis in colon adenocarcinoma.Frontiers in oncology · 2023Article
- Subtype-based analysis of cell-in-cell structures in non-small cell lung cancer.American journal of cancer research · 2023Article
- CEMIP promotes extracellular matrix-detached prostate cancer cell survival by inhibiting ferroptosis.Cancer science · 2022Article
- Chronic Leptin Treatment Induces Epithelial-Mesenchymal Transition in MCF10A Mammary Epithelial Cells.Journal of mammary gland biology and neoplasia · 2022Article
- A century of programmed cell death in the ovary: a commentary.Journal of assisted reproduction and genetics · 2022Article
- Review
- 4.1N-Mediated Interactions and Functions in Nerve System and Cancer.Frontiers in molecular biosciences · 2021Review
- Entosis: From Cell Biology to Clinical Cancer Pathology.Cancers · 2020Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Epithelial ovarian cancer (EOC) is one of the leading causes of death from gynecologic cancers and peritoneal dissemination is the major cause of death in patients with EOC. Although the loss of 4.1N is associated with increased risk of malignancy, its association with EOC remains unclear. To explore the underlying mechanism of the loss of 4.1N in constitutive activation of epithelial-mesenchymal transition (EMT) and matrix-detached cell death resistance, we investigated samples from 268 formalin-fixed EOC tissues and performed various in vitro and in vivo assays. We report that the loss of 4.1N correlated with progress in clinical stage, as well as poor survival in EOC patients. The loss of 4.1N induces EMT in adherent EOC cells and its expression inhibits anoikis resistance and EMT by directly binding and accelerating the degradation of 14-3-3 in suspension EOC cells. Furthermore, the loss of 4.1N could increase the rate of entosis, which aggravates cell death resistance in suspension EOC cells. Moreover, xenograft tumors in nude mice also show that the loss of 4.1N can aggravate peritoneal dissemination of EOC cells. Single-agent and combination therapy with a ROCK inhibitor and a 14-3-3 antagonist can reduce tumor spread to varying degrees. Our results not only define the vital role of 4.1N loss in inducing EMT, anoikis resistance, and entosis-induced cell death resistance in EOC, but also suggest that individual or combined application of 4.1N, 14-3-3 antagonists, and entosis inhibitors may be a promising therapeutic approach for the treatment of EOC.
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