ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2014
Functional MUC4 suppress epithelial-mesenchymal transition in lung adenocarcinoma metastasis.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 21 citations in OpenAlex.
- Synergistic Profiling of Programmed Cell Death and Immune Responses Identifies a Novel Prognostic Index for Cervical Cancer.ACS omega · 2026Article
- Transmembrane mucins in lung adenocarcinoma: understanding of current molecular mechanisms and clinical applications.Cell death discovery · 2025Review
- Immune-related gene characteristics: A new chapter in precision treatment of gastric cancer.World journal of gastrointestinal oncology · 2024Article
- Article
- The role of membrane mucin MUC4 in breast cancer metastasis.Endocrine-related cancer · 2021Review
- PRDM16 functions as a suppressor of lung adenocarcinoma metastasis.Journal of experimental & clinical cancer research : CR · 2019Article
- Review
- Mucin-1 correlates with survival, smoking status, and growth patterns in lung adenocarcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- Mucins and Wnt/β-catenin signaling in gastrointestinal cancers: an unholy nexus.Carcinogenesis · 2016Review
- Long Noncoding RNA-LET Suppresses Tumor Growth and EMT in Lung Adenocarcinoma.BioMed research international · 2016Article
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8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mucin MUC4 is a high molecular weight membrane-bound transmembrane glycoprotein that is frequently detected in invasive and metastatic cancer. The overexpression of MUC4 is associated with increased risks for several types of cancer. However, the functional role of MUC4 is poorly understood in lung adenocarcinoma. Using antisense-MUC4-RNA transfected adenocarcinoma cells, we discovered that the loss of MUC4 expression results in epithelial-mesenchymal transition (EMT). We found morphological alterations and the repression of the epithelial marker E-cadherin in transfected cells. Additionally, the loss of MUC4 caused the upregulation of the mesenchymal marker vimentin compared to control cells. Using a MUC4-knockdown versus control LTEP xenograft mice model (129/sv mice), we also found that EMT happened in lung tissues of MUC4-knockdown-LTEP xenograft mice. Moreover, antisense-MUC4-RNA transfected cells had a significantly increased cellular migration ability in vitro. The loss of MUC4 also occurred in lung adenocarcinoma patients with lymph node metastases. We further investigated MUC4 and found that it plays a critical role in regulating EMT by modulating β-catenin. Taken together, our study reveals a novel role for MUC4 in suppressing EMT and suggests that the assessment of MUC4 may function as a prognostic biomarker and could be a potential therapeutic target for lung adenocarcinoma metastasis.
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