ArticleOncogene2010
MUC4 mucin-induced epithelial to mesenchymal transition: a novel mechanism for metastasis of human ovarian cancer cells.
Article in Oncogene, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 77 papers.
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Who cites it
77 citing papers in PubMed, 137 citations in OpenAlex.
- Selective inhibition of ALDH1A3 impedes breast cancer growth and metastasis by blocking ALDH1A3-driven transcriptional programs.iScience · 2026Article
- MUC4 mutations promote a thrombotic phenotype in patients with paroxysmal nocturnal haemoglobinuria by increasing the deposition of terminal complement.Clinical and translational medicine · 2026Article
- MK2-mediated AKT/MYC signaling activation promotes epithelial-mesenchymal transition in lung adenocarcinoma.Frontiers in genetics · 2025Article
- Ovarian serous carcinoma with stomach metastasis: a rare case report and literature review.The Journal of international medical research · 2024Review
- Research progress of epithelial-mesenchymal transformation-related transcription factors in peritoneal metastases.Journal of Cancer · 2024Review
- RUNX1-MUC13 Interaction Activates Wnt/β-Catenin Signaling Implications for Colorectal Cancer Metastasis.International journal of biological sciences · 2024Article
- [Role and clinical significance of MUC4 gene mutations in thrombotic events in patients with classic paroxysmal nocturnal hemoglobinuria].Zhonghua xue ye xue za zhi = Zhonghua xueyexue zazhi · 2023Article
- LACTB exerts tumor suppressor properties in epithelial ovarian cancer through regulation of Slug.Life science alliance · 2023Article
- Protein Glycosylation as Biomarkers in Gynecologic Cancers.Diagnostics (Basel, Switzerland) · 2022Review
- Extracellular vesicles in ovarian cancer chemoresistance, metastasis, and immune evasion.Cell death & disease · 2022Review
- Role and mechanism of miR-211 in human cancer.Journal of Cancer · 2022Review
- The role of membrane mucin MUC4 in breast cancer metastasis.Endocrine-related cancer · 2021Review
- Mucins reprogram stemness, metabolism and promote chemoresistance during cancer progression.Cancer metastasis reviews · 2021Review
- New Actors Driving the Epithelial-Mesenchymal Transition in Cancer: The Role of Leptin.Biomolecules · 2020Review
- Acinar transformed ductal cells exhibit differential mucin expression in a tamoxifen-induced pancreatic ductal adenocarcinoma mouse model.Biology open · 2020Article
- Tepotinib Inhibits the Epithelial-Mesenchymal Transition and Tumor Growth of Gastric Cancers by Increasing GSK3β, E-Cadherin, and Mucin 5AC and 6 Levels.International journal of molecular sciences · 2020Article
- Current insights into the metastasis of epithelial ovarian cancer - hopes and hurdles.Cellular oncology (Dordrecht, Netherlands) · 2020Review
- Relationship between neuropilin-1 expression and prognosis, according to gastric cancer histology.Journal of molecular histology · 2020Article
- A Population-Based Study on Liver Metastases in Women With Newly Diagnosed Ovarian Cancer.Frontiers in oncology · 2020Article
- Molecular biology and immunology of gastric cancer peritoneal metastasis.Translational gastroenterology and hepatology · 2020Review
17 more citing papers are in PubMed but not listed here.
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
The acquisition of invasiveness in ovarian cancer (OC) is accompanied by the process of epithelial-to-mesenchymal transition (EMT). The MUC4 mucin is overexpressed in ovarian tumors and has a role in the invasiveness of OC cells. The present study was aimed at evaluating the potential involvement of MUC4 in the metastasis of OC cells by inducing EMT. Ectopic overexpression of MUC4 in OC cells (SKOV3-MUC4) resulted in morphological alterations along with a decreased expression of epithelial markers (E-cadherin and cytokeratin (CK)-18) and an increased expression of mesenchymal markers (N-cadherin and vimentin) compared with the control cells (SKOV3-vector). Also, pro-EMT transcription factors TWIST1, TWIST2 and SNAIL showed an upregulation in SKOV3-MUC4 cells. We further investigated the pathways upstream of N-cadherin, such as focal adhesion kinase (FAK), MKK7, JNK1/2 and c-Jun, which were also activated in the SKOV3-MUC4 cells compared with SKOV3-vector cells. Inhibition of phospho-FAK (pFAK) and pJNK1/2 decreased N-cadherin expression in the MUC4-overexpressing cells, which further led to a significant decrease in cellular motility. Knockdown of N-cadherin decreased the activation of extracellular signal-regulated kinase-1/2 (ERK1/2), AKT and matrix metalloproteinase 9 (MMP9), and inhibited the motility in the SKOV3-MUC4 cells. Upon in vivo tumorigenesis and metastasis analysis, the SKOV3-MUC4 cells produced significantly larger tumors and demonstrated a higher incidence of metastasis to distance organs (peritoneal wall, colon, intestine, stomach, lymph nodes, liver and diaphragm). Taken together, our study reveals a novel role for MUC4 in inducing EMT through the upregulation of N-cadherin and promoting metastasis of OC cells.
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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.