ArticleOncogenesis2018
MUC13 contributes to rewiring of glucose metabolism in pancreatic cancer.
Article in Oncogenesis, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 47 citations in OpenAlex.
- Signatures of Pancreatic Ductal Adenocarcinoma Uncovered by Integrative Multi-Omics Analysis.Cancers · 2026Article
- Transcriptome analysis of goat adipose tissue-derived mesenchymal stem cells cultured in variable oxygen conditions.Frontiers in cell and developmental biology · 2026Article
- MUC13-Associated Molecular Interactome in Pancreatic Cancer.Computational and structural biotechnology journal · 2026Article
- MUC13 is a crucial player in YAP1-β-catenin survival complex mediated cancer metastasis.Frontiers in medicine · 2025Article
- Article
- Deciphering cellular and molecular mechanism of MUC13 mucin involved in cancer cell plasticity and drug resistance.Cancer metastasis reviews · 2024Review
- RUNX1-MUC13 Interaction Activates Wnt/β-Catenin Signaling Implications for Colorectal Cancer Metastasis.International journal of biological sciences · 2024Article
- Advances in Drug Therapy for Metastatic Pancreatic Ductal Adenocarcinoma.Journal of Cancer · 2024Review
- MUC13 drives cancer aggressiveness and metastasis through the YAP1-dependent pathway.Life science alliance · 2023Article
- MUC13 promotes the development of esophageal cancer by upregulating the expression of O-glycan process-related molecules.Discover oncology · 2023Article
- Integrative big transcriptomics data analysis implicates crucial role of MUC13 in pancreatic cancer.Computational and structural biotechnology journal · 2023Article
- Reprogramming of pancreatic adenocarcinoma immunosurveillance by a microbial probiotic siderophore.Communications biology · 2022Article
- Review
- MUC13 promotes lung cancer development and progression by activating ERK signaling.Oncology letters · 2022Article
- Steviol Represses Glucose Metabolism and Translation Initiation in Pancreatic Cancer Cells.Biomedicines · 2021Article
- Article
- Mucins reprogram stemness, metabolism and promote chemoresistance during cancer progression.Cancer metastasis reviews · 2021Review
- Strain-based and sex-biased differences in adrenal and pancreatic gene expression between KK/HlJ and C57BL/6 J mice.BMC genomics · 2021Article
- Pancreatic cancer and adaptive metabolism in a nutrient-deficient environment.Central-European journal of immunology · 2021Review
- Emerging Kinase Therapeutic Targets in Pancreatic Ductal Adenocarcinoma and Pancreatic Cancer Desmoplasia.International journal of molecular sciences · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Pancreatic tumors are rewired for high-glucose metabolism and typically present with exceptionally poor prognosis. Recently, we have shown that MUC13, which is highly expressed in pancreatic tumors, promotes tumor progression via modulation of HER2 receptor tyrosine kinase activity. Herein, we investigate a novel, MUC13-mediated molecular mechanism responsible for higher glucose metabolism in pancreatic tumors. Our results demonstrate that MUC13 expression leads to the activation/nuclear translocation of NF-κB p65 and phosphorylation of IκB, which in turn upregulates the expression of important proteins (Glut-1, c-Myc, and Bcl-2) that are involved in glucose metabolism. MUC13 functionally interacts and stabilizes Glut-1 to instigate downstream events responsible for higher glucose uptake in pancreatic cancer cells. Altered MUC13 expression by overexpression and knockdown techniques effectively modulated glucose uptake, lactate secretion, and metastatic phenotypes in pancreatic cancer cells. NF-κB inhibitor, Sulfasalazine, abrogates the MUC13 and Glut-1 interaction, and attenuates events associated with MUC13-induced glucose metabolism. Pancreatic ductal adenocarcinoma (PDAC) patient tissue samples also show a positive correlation between the expression of these two proteins. These results delineate how MUC13 rewire aberrant glucose metabolism to enhance aggressiveness of pancreatic cancer and revealed a novel mechanism to develop newer therapeutic strategies for this exceptionally difficult cancer.
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.