ArticleMolecular cancer2017
Targeting MUC1-C inhibits the AKT-S6K1-elF4A pathway regulating TIGAR translation in colorectal cancer.
Article in Molecular cancer, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03467308 (Identification of New Signaling Pathways Targeting Colorectal Cancer in Egyptian Patients), which is not on this map. Cited by 35 papers.
What it found
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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.
Identification of New Signaling Pathways Targeting Colorectal Cancer in Egyptian Patients
Who cites it
35 citing papers in PubMed, 64 citations in OpenAlex.
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- Tumour-Associated MUC1 Exerts Multiple Effects on Cholesterol and Lipid Metabolism-A Potential Pathogenic Effector of Atherosclerosis in Cancer.International journal of molecular sciences · 2026Article
- Lack of intestinal Mucin-1 impairs intestinal epithelial barrier and promotes metabolic dysfunction-associated steatotic liver disease in male mice.Nature communications · 2025Article
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- Improved breast cancer diagnosis using a CA15-3 capture antibody-lectin sandwich assay.Breast cancer research and treatment · 2025Article
- The Pentose Phosphate Pathway: From Mechanisms to Implications for Gastrointestinal Cancers.International journal of molecular sciences · 2025Review
- In vivo Therapeutic Inhibition of the Tp53-Induced Glycolysis and Apoptosis Regulator (TIGAR) by Intravenous Administration of an Anti-Oncological siRNA-Biopolymer, TI6752 (Tituxistatin), in a Preclinical Xenograft Model of Colorectal Cancer.Journal of experimental pharmacology · 2025Article
- High-throughput neural stem cell-based drug screening identifies S6K1 inhibition as a selective vulnerability in sonic hedgehog-medulloblastoma.Neuro-oncology · 2024Article
- Immune landscape of hepatocellular carcinoma: The central role of TP53-inducible glycolysis and apoptosis regulator.Open medicine (Warsaw, Poland) · 2024Article
- Unraveling the role of C1GALT1 in abnormal glycosylation and colorectal cancer progression.Frontiers in oncology · 2024Review
- Expanded Alternatives of CRISPR-Cas9 Applications in Immunotherapy of Colorectal Cancer.Molecular diagnosis & therapy · 2024Review
- MUC1-C integrates aerobic glycolysis with suppression of oxidative phosphorylation in triple-negative breast cancer stem cells.iScience · 2023Article
- TIGAR Protects Cochlear Hair Cells against Teicoplanin-Induced Damage.Molecular neurobiology · 2023Article
- Article
- Glycosylated modification of MUC1 maybe a new target to promote drug sensitivity and efficacy for breast cancer chemotherapy.Cell death & disease · 2022Article
- The progress of protein synthesis factors eIFs, eEFs and eRFs in inflammatory bowel disease and colorectal cancer pathogenesis.Frontiers in oncology · 2022Review
- Novel insights into the roles and therapeutic implications of MUC1 oncoprotein via regulating proteins and non-coding RNAs in cancer.Theranostics · 2022Review
- Mucinous adenocarcinoma: A unique clinicopathological subtype in colorectal cancer.World journal of gastrointestinal surgery · 2021Review
- Mucin1 and Mucin16: Therapeutic Targets for Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
7 authors at 5 institutions in 3 countries.
Funding
Abstract
backgroundColorectal cancer is third most common malignancy and is the second most common cause of cancer-related death. The MUC1 heterodimeric protein is aberrantly overexpressed in colorectal cancer and has been linked to poor outcomes in this disease. Here, we investigate the effects of the MUC1-C subunit inhibitor (GO-203), which disrupts MUC1-C homo-oligomerization, on human colorectal cancer cells.
methodsTIGAR mRNA level was determined using qRT-PCR. Western blotting was used to measure TIGAR protein level and AKT-mTOR-S6K1 pathways. Reactive oxygen species and apoptosis were measured by flow cytometry. Effect of MUC1-C peptide, GO-203 was studied on colorectal xenograft tumors. Immunohistochemistry was utilized for TIGAR staining.
resultsTreatment of MUC1-overexpressing SKCO-1 and Colo-205 colon cancer cells with GO-203 was associated with downregulation of the TP53-inducible glycolysis and apoptosis regulator (TIGAR) protein. TIGAR promotes the shunting of glycolytic intermediates into the pentose phosphate pathway and thus is of importance for maintaining redox balance. We show that GO-203-induced suppression of TIGAR is mediated by inhibition of AKT and the downstream mTOR pathway. The results also demonstrate that targeting MUC1-C blocks eIF4A cap-dependent translation of TIGAR. In concert with these results, GO-203-induced suppression of TIGAR was associated with decreases in GSH levels. GO-203 treatment also resulted in increases in reactive oxygen species (ROS) and loss of mitochondrial transmembrane potential. Consistent with these results, GO-203 inhibited the growth of colon cancer cells in vitro and as xenografts in nude mice. Inhibition of MUC1-C also downregulated TIGAR expression in xenograft tissues.
conclusionsThese findings indicate that MUC1-C is a potential target for the treatment of colorectal cancer. Colorectal cancer patients who overexpress MUC1-C may be candidates for treatment with the MUC1-C inhibitor alone or in combination therapy with other agents.
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