ArticleMolecular oncology2019
Molecular evidence of field cancerization initiated by diabetes in colon cancer patients.
Article in Molecular oncology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 16 citations in OpenAlex.
- The Crosstalk Between YAP/TAZ and Cancer Metabolism: From Mechanistic Insights to Drug Discovery.International journal of molecular sciences · 2026Review
- Mechanism of AGEs-RAGE axis inhibition of ferroptosis in type 2 diabetic colon cancer by regulatory CEACAM1.Scientific reports · 2026Article
- NMolecular medicine reports · 2026Article
- Identification of diabetes-related signatures as prognostic and therapeutic biomarkers in colon cancer.Discover oncology · 2025Article
- Recent Insights Into Breast Cancer: Molecular Pathways, Epigenetic Regulation, and Emerging Targeted Therapies.Breast cancer : basic and clinical research · 2025Review
- Hippo/YAP signaling pathway: a new therapeutic target for diabetes mellitus and vascular complications.Therapeutic advances in endocrinology and metabolism · 2023Review
- Field cancerization in breast cancer.The Journal of pathology · 2022Review
- Global mapping of cancers: The Cancer Genome Atlas and beyond.Molecular oncology · 2021Review
- Impact of preoperative antibiotics and other variables on integrated microbiome-host transcriptomic data generated from colorectal cancer resections.World journal of gastroenterology · 2021Article
- Proteomics Analysis of Gastric Cancer Patients with Diabetes Mellitus.Journal of clinical medicine · 2021Article
- Oleic Acid and Insulin as Key Characteristics of T2D Promote Colorectal Cancer Deterioration in Xenograft Mice Revealed by Functional Metabolomics.Frontiers in oncology · 2021Article
- Correlation between Expression Profiles of Key Signaling Genes in Colorectal Cancer Samples from Type 2 Diabetic and Non-Diabetic Patients.Life (Basel, Switzerland) · 2020Article
- Mechanism of miR-98 inhibiting tumor proliferation and invasion by targeting IGF1R in diabetic patients combined with colon cancer.Oncology letters · 2020Article
- Hyperglycemia Associated Metabolic and Molecular Alterations in Cancer Risk, Progression, Treatment, and Mortality.Cancers · 2019Review
- Diabetes-mediated promotion of colon mucosa carcinogenesis is associated with mitochondrial dysfunction.Molecular oncology · 2019Article
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Authors and funding
22 authors at 5 institutions in 1 country.
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Abstract
The potential involvement of type 2 diabetes mellitus (T2DM) as a risk factor for colon cancer (CC) has been previously reported. While several clinical studies show a higher incidence of CC and a lower survival rate in diabetics, others report no association. Our own experience indicates that diabetes does not seem to worsen the prognosis once the tumor is present. Despite this controversy, there are no wide-spectrum molecular studies that delve into the impact of T2DM-related mechanisms in colon carcinogenesis. Here, we present a transcriptomic and proteomic profiling of paired tumor and normal colon mucosa samples in a cohort of 42 CC patients, 23 of which have T2DM. We used gene set enrichment and network approaches to extract relevant pathways in diabetics, referenced them to current knowledge, and tested them using in vitro techniques. Through our transcriptomics approach, we identified an unexpected overlap of pathways overrepresented in diabetics compared to nondiabetics, in both tumor and normal mucosa, including diabetes-related metabolic and signaling processes. Proteomic approaches highlighted several cancer-related signaling routes in diabetics found only in normal mucosa, not in tumors. An integration of the transcriptome and proteome analyses suggested the deregulation of key pathways related to colon carcinogenesis which converged on tumor initiation axis TEAD/YAP-TAZ as a potential initiator of the process. In vitro studies confirmed upregulation of this pathway in nontumor colon cells under high-glucose conditions. In conclusion, T2DM associates with deregulation of cancer-related processes in normal colon mucosa adjacent to tissue which has undergone a malignant transformation. These data support that in diabetic patients, the local microenvironment in normal colon mucosa may be a factor driving field cancerization promoting carcinogenesis. Our results set a new framework to study links between diabetes and colon cancer, including a new role of the TEAD/YAP-TAZ complex as a potential driver.
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