ArticleOncogene2017
Core 3 mucin-type O-glycan restoration in colorectal cancer cells promotes MUC1/p53/miR-200c-dependent epithelial identity.
Article in Oncogene, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
What it found
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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.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Pooled it
- Restoring O-glycosylation and expression of MUC2 limits progression of colorectal cancer.Cell death & disease · 2026Article
- Exercise-secreted antitumor myokines: mechanistic insights and translational potential.Frontiers in sports and active living · 2026Review
- Resveratrol and p53: How are they involved in CRC plasticity and apoptosis?Journal of advanced research · 2024Review
- Mucin 1 expression is regulated by hsa_circ_0055054/microRNA‑122‑5p and promotes hepatocellular carcinoma development.Oncology letters · 2024Article
- Impacts of β-1, 3-N-acetylglucosaminyltransferases (B3GNTs) in human diseases.Molecular biology reports · 2024Review
- Review
- MicroRNA-10a-5p-mediated downregulation of GATA6 inhibits tumor progression in ovarian cancer.Human cell · 2024Article
- Unraveling the role of C1GALT1 in abnormal glycosylation and colorectal cancer progression.Frontiers in oncology · 2024Review
- YAP1 expression in colorectal cancer confers the aggressive phenotypes via its target genes.Cell cycle (Georgetown, Tex.) · 2024Article
- The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023Review
- MUC13 promotes the development of esophageal cancer by upregulating the expression of O-glycan process-related molecules.Discover oncology · 2023Article
- The Mutual Relationship between Glycosylation and Non-Coding RNAs in Cancer and Other Physio-Pathological Conditions.International journal of molecular sciences · 2022Review
- Clinicopathologic and genomic characteristics of mucinous gastric adenocarcinoma.Gastric cancer : official journal of the International Gastric Cancer Association and the Japanese Gastric Cancer Association · 2022Article
- Estradiol-mediated inhibition of DNMT1 decreases p53 expression to induce M2-macrophage polarization in lung cancer progression.Oncogenesis · 2022Article
- LSD1 regulates the FOXF2-mediated Wnt/β-catenin signaling pathway by interacting with Ku80 to promote colon cancer progression.American journal of cancer research · 2022Article
- Novel insights into the roles and therapeutic implications of MUC1 oncoprotein via regulating proteins and non-coding RNAs in cancer.Theranostics · 2022Review
- Association between the expression of core 3 synthase and survival outcomes of patients with cholangiocarcinoma.Oncology letters · 2021Article
- Glycobiology of the Epithelial to Mesenchymal Transition.Biomedicines · 2021Review
- Robust Glycogene-Based Prognostic Signature for Proficient Mismatch Repair Colorectal Adenocarcinoma.Frontiers in oncology · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The attachment of cell-surface carbohydrates to proteins mediated by the amino acids serine or threonine (O-glycan) is involved in tumor metastasis; the roles of O-glycans vary depending on their structure, but the detailed mechanisms by which O-glycans trigger signaling to control tumor metastasis are largely unknown. In this study, we found that the reduced expression of core 3 synthase correlated with metastasis to lymph nodes and distant organs, resulting in poor prognosis for colorectal cancer (CRC) patients. Mechanically, we revealed that mucin-type core 3 O-glycan was synthesized at the membrane-tethered MUC1 N terminus because of core 3 synthase expression in colon cancer cells. This further inhibited the translocation of MUC1-C to the nucleus, initiated p53 gene transcription that was dependent on the inhibition of MUC1-C nucleus translocation, activated p53-mediated miR-200c expression and resulted in mesenchymal-epithelial transition (MET). Inhibition of MUC1 via small interfering RNA (siRNA) in re-expressed core 3 synthase colon cancer cells further inhibited MUC1-C nucleus translocation, increased p53 and miR-200c expression, and enhanced MET. However, inhibition of p53 via siRNA or miR-200c via miR-200c inhibitor in re-expressed core 3 synthase colon cancer cells promoted the epithelial-mesenchymal transition (EMT) in a reversible manner. Core 3 synthase mRNA levels and the p53 mRNA levels or miR-200c levels in the colon cancerous samples were positively correlated. Our findings suggest a novel mechanism linking mucin-type core 3 O-glycan to the EMT-MET plasticity of CRC cells via MUC1/p53/miR-200c-dependent signaling cascade and shed light on therapeutic strategies to treat this malignancy.
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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.