ArticlePloS one2015
Expression of the Carboxy-Terminal Portion of MUC16/CA125 Induces Transformation and Tumor Invasion.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 54 citations in OpenAlex.
- Chronic Medical Conditions and CA125 Levels among Women without Ovarian Cancer.Cancer epidemiology, biomarkers & prevention : a publication of the American Association for Cancer Research, cosponsored by the American Society of Preventive Oncology · 2018Trial
- A monoclonal antibody W1 blocks mesothelin-mediated tumor progression.Molecular therapy. Oncology · 2026Article
- An endoplasmic reticulum stress- and Golgi apparatus-related signature reveals immune microenvironment remodeling andFrontiers in immunology · 2026Article
- Hypoxia induced VEGF secretion promotes resistance to bispecific T-cell engagers.Signal transduction and targeted therapy · 2025Article
- Microbiome and Metaproteome of Craniofacial Implant Regions in Health and Disease.Oral diseases · 2025Article
- Mapping the Binding Sites of CA125-Specific Antibodies on a Revised Molecular Model of MUC16.Cancers · 2025Article
- Muc16CD is a novel CAR T cell target antigen for the treatment of pancreatic cancer.Molecular therapy. Oncology · 2024Article
- Targeting Galectin 3 illuminates its contributions to the pathology of uterine serous carcinoma.British journal of cancer · 2024Article
- Structural basis for antibody recognition of the proximal MUC16 ectodomain.Journal of ovarian research · 2024Article
- Virus-like particle vaccine displaying an external, membrane adjacent MUC16 epitope elicits ovarian cancer-reactive antibodies.Journal of ovarian research · 2024Article
- Unveiling the Immunogenicity of Ovarian Tumors as the Crucial Catalyst for Therapeutic Success.Cancers · 2023Review
- Blood Plasma Small Non-Coding RNAs as Diagnostic Molecules for the Progesterone-Receptor-Negative Phenotype of Serous Ovarian Tumors.International journal of molecular sciences · 2023Article
- Targeting galectin-driven regulatory circuits in cancer and fibrosis.Nature reviews. Drug discovery · 2023Review
- Review
- CAR-T Cells in the Treatment of Ovarian Cancer: A Promising Cell Therapy.Biomolecules · 2023Review
- Molecular Classification of Genes Associated with Hypoxic Lipid Metabolism in Pancreatic Cancer.Biomolecules · 2022Article
- Dual Fluorescence Isogenic Synthetic Lethal Kinase Screen and High-Content Secondary Screening for MUC16/CA125-Selective Agents.Molecular cancer therapeutics · 2022Article
- Human iPSC-derived fallopian tube organoids with BRCA1 mutation recapitulate early-stage carcinogenesis.Cell reports · 2021Article
- Predictive effects of preoperative serum CA125 and AFP levels on post-hepatectomy survival in patients with hepatitis B-related hepatocellular carcinoma.Oncology letters · 2021Article
- Targeting galectin-3 with a high-affinity antibody for inhibition of high-grade serous ovarian cancer and other MUC16/CA-125-expressing malignancies.Scientific reports · 2021Article
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
The CA125 antigen is found in the serum of many patients with serous ovarian cancer and has been widely used as a disease marker. CA125 has been shown to be an independent factor for clinical outcome in this disease. In The Cancer Genome Atlas ovarian cancer project, MUC16 expression levels are frequently increased, and the highest levels of MUC16 expression are linked to a significantly worse survival. To examine the biologic effect of the proximal portion of MUC16/CA125, NIH/3T3 (3T3) fibroblast cell lines were stably transfected with the carboxy elements of MUC16. As few as 114 amino acids from the carboxy-terminal portion of MUC16 were sufficient to increase soft agar growth, promote matrigel invasion, and increase the rate of tumor growth in athymic nude mice. Transformation with carboxy elements of MUC16 was associated with activation of the AKT and ERK pathways. MUC16 transformation was associated with up-regulation of a number of metastases and invasion gene transcripts, including IL-1β, MMP2, and MMP9. All observed oncogenic changes were exclusively dependent on the extracellular "ectodomain" of MUC16. The biologic impact of MUC16 was also explored through the creation of a transgenic mouse model expressing 354 amino acids of the carboxy-terminal portion of MUC16 (MUC16c354). Under a CMV, early enhancer plus chicken β actin promoter (CAG) MUC16c354 was well expressed in many organs, including the brain, colon, heart, kidney, liver, lung, ovary, and spleen. MUC16c354 transgenic animals appear to be viable, fertile, and have a normal lifespan. However, when crossed with p53-deficient mice, the MUC16c354:p53+/- progeny displayed a higher frequency of spontaneous tumor development compared to p53+/- mice alone. We conclude that the carboxy-terminal portion of the MUC16/CA125 protein is oncogenic in NIH/3T3 cells, increases invasive tumor properties, activates the AKT and ERK pathways, and contributes to the biologic properties of ovarian cancer.
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