ArticleDigestive diseases and sciences2022
Mucin 16 Promotes Colorectal Cancer Development and Progression Through Activation of Janus Kinase 2.
Article in Digestive diseases and sciences, 2022. 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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17 citing papers in PubMed, 20 citations in OpenAlex.
- Loss of ST8SIA6 is associated with enhanced MUC16-Integrin β4 signaling and aggressive phenotypes in colorectal cancer.Biochemistry and biophysics reports · 2026Article
- Loss of SATB2 is associated with MUC16 upregulation in the invasive component of colitis-associated colorectal carcinoma.Virchows Archiv : an international journal of pathology · 2026Article
- The Role of Gut Microbiota and Mucin Barrier in the Pathogenesis of Colorectal Cancer.Current issues in molecular biology · 2025Review
- Genomic characterization of patients with colorectal cancer.Hereditary cancer in clinical practice · 2025Article
- Whole-exome sequencing identifies new pathogenic germline variants in patients with colorectal polyposis.World journal of gastroenterology · 2025Article
- Hormonally upregulated neu tumor-associated kinase (HUNK) modulates gastric cancer progression through the regulation of cell homeostasis.Cell communication and signaling : CCS · 2025Article
- Mesothelin expression correlates with elevated inhibitory immune activity in patients with colorectal cancer.Cancer gene therapy · 2024Article
- Article
- Single-cell analysis of matrisome-related genes in breast invasive carcinoma: new avenues for molecular subtyping and risk estimation.Frontiers in immunology · 2024Article
- Mesothelin expression correlates with elevated inhibitory immune activity in patients with colorectal cancer.Research square · 2023Article
- Review
- Review
- View from the Biological Property: Insight into the Functional Diversity and Complexity of the Gut Mucus.International journal of molecular sciences · 2023Review
- Expression of MUC16/CA125 Is Associated with Impaired Survival in Patients with Surgically Resected Cholangiocarcinoma.Cancers · 2022Article
- [MUC16: The Novel Target for Tumor Therapy].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2022Review
- Article
- Whole genome sequencing of Malaysian colorectal cancer patients reveals specific druggable somatic mutations.Frontiers in molecular biosciences · 2022Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMucin 16 (MUC16), a cell surface-associated mucin, has been implicated to be upregulated in a large repertoire of malignances. However, its function in the pathogenesis of colorectal cancer (CRC) is unknown.
aimsHere, we explored the regulatory role of MUC16 in CRC.
methodsFirst, tumor and paracancerous tissues, and serum samples from 162 CRC patients, peripheral blood samples from 48 healthy volunteers and 72 benign colorectal patients were collected. The correlation between the MUC16 expression and the clinical phenotypes of the patients was analyzed. Subsequently, HCT116 and SW480 cells with deletion of MUC16 were established to detect changes in the growth and metastatic capacities of CRC cells. The genes with the highest correlation with MUC16 were predicted by bioinformatics, and their binding relationships were detected by Co-IP and double-labeled immunofluorescence, followed by functional rescue experiments.
resultsOverexpression of MUC16 in CRC patients was positively correlated with serum biomarkers and poor prognosis of patients. It was demonstrated by in vitro and in vivo experiments that knocking-down the expression of MUC16 could significantly inhibit the growth and metastasis of CRC cells. MUC16 activated janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) by interacting with JAK2. Further overexpression of JAK2 in cells with poor expression of MUC16 revealed a significant increase in the proliferative and metastatic capacities of CRC cells.
conclusionsMUC16 contributes to the development and progression of CRC by binding to JAK2, thereby promoting phosphorylation of JAK2 and further activating STAT3 phosphorylation.
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