ArticleJournal of experimental & clinical cancer research : CR2016
The role of the AMOP domain in MUC4/Y-promoted tumour angiogenesis and metastasis in pancreatic cancer.
Article in Journal of experimental & clinical cancer research : CR, 2016. 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 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- High serum isthmin-1 as a biomarker for the progression of renal function decline in patients with type 2 diabetes mellitus.BMC endocrine disorders · 2025Article
- The Role of Mucins in Cancer and Cancer Progression: A Comprehensive Review.Current issues in molecular biology · 2025Review
- Crystal structure of Isthmin-1 and reassessment of its functional role in pre-adipocyte signaling.Nature communications · 2025Article
- Oncogenic KRAS, Mucin 4, and Activin A-Mediated Fibroblast Activation Cooperate for PanIN Initiation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2023Article
- Article
- Advances in research of biological functions of Isthmin-1.Journal of cell communication and signaling · 2023Review
- Isthmin-1 (Ism1) modulates renal branching morphogenesis and mesenchyme condensation during early kidney development.Nature communications · 2023Article
- Article
- A prediction model integrated genomic alterations and immune signatures of tumor immune microenvironment for early recurrence of stage I NSCLC after curative resection.Translational lung cancer research · 2022Article
- The role of membrane mucin MUC4 in breast cancer metastasis.Endocrine-related cancer · 2021Review
- Mucins as anti-cancer targets: perspectives of the glycobiologist.Glycoconjugate journal · 2021Review
- The Role of Notch3 Signaling in Cancer Stemness and Chemoresistance: Molecular Mechanisms and Targeting Strategies.Frontiers in molecular biosciences · 2021Review
- Article
- Epigenetic Modification of CFTR in Head and Neck Cancer.Journal of clinical medicine · 2020Article
- ISM1 regulates NODAL signaling and asymmetric organ morphogenesis during development.The Journal of cell biology · 2019Article
- Axed MUC4 (MUC4/X) aggravates pancreatic malignant phenotype by activating integrin-β1/FAK/ERK pathway.Biochimica et biophysica acta. Molecular basis of disease · 2018Article
- The Role ofThe oncologist · 2018Review
- Decreased WWOX expression promotes angiogenesis in osteosarcoma.Oncotarget · 2017Article
- Genetic variants of mucins: unexplored conundrum.Carcinogenesis · 2017Review
- MUC4 mucin- a therapeutic target for pancreatic ductal adenocarcinoma.Expert opinion on therapeutic targets · 2017Review
Corrections and comments
- Erratum issued
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMUC4 is a high molecular weight membrane protein that is overexpressed in pancreatic cancer (PC) and is associated with the development and progression of this disease. However, the exact mechanisms through which MUC4 domains promote these biological processes have rarely been studied, partly because of its high molecular weight, difficulty to overexpress it. Here, we use MUC4/Y, one of the MUC4 transcript variants, as a model molecule to investigate the AMOP-domain of MUC4(MUC/Y).
methodsWe used cell proliferation, migration, invasion and tube formation assays in vitro to explore the abilities of AMOP domain in PC. In vivo, the matrigel plug assay, orthotopic implantation and Kaplan-Meier survival curves were used to check the results we observed in vitro. Finally, we discovered the underlying mechanism through western blot and immunofluorescence.
resultsWe found that MUC4/Y overexpression could enhance the angiogenic and metastatic properties of PC cells, both in vitro and in vivo. However, the deletion of AMOP domain could cutback these phenomena. Additionally, Kaplan-Meier survival curves showed that mice injected with MUC4/Y overexpressed cells had shorter survival time, compared with empty-vector-transfected cells (MUC4/Y-EV), or cells expressing MUC4/Y without the AMOP domain (MUC4/Y-AMOP(△)). Our data also showed that overexpression of MUC4/Y could activate NOTCH3 signaling, increasing the expression of downstream genes: VEGF-A, MMP-9 and ANG-2.
conclusionsThe AMOP domain had an important role in MUC4/Y (MUC4)-mediated tumour angiogenesis and metastasis of PC cells; and the NOTCH3 signaling was involved. These findings provided new insights into PC therapies. Our study also supplies a new method to study other high molecular membrane proteins.
Indexed as
Identifiers
What OpenQuestion holds
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.