ArticleJournal of cellular physiology2019
Inhibition of MUC1-C regulates metabolism by AKT pathway in esophageal squamous cell carcinoma.
Article in Journal of cellular physiology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 36 citations in OpenAlex.
- The network map of mucin 1 mediated signaling in cancer progression and immune modulation.Discover oncology · 2025Article
- Mucin-1: a promising pan-cancer therapeutic target.NPJ precision oncology · 2025Review
- Pharmacological Modulation of MutantBiomedicines · 2025Review
- Mucins as Precision Biomarkers in Glioma: Emerging Evidence for Their Potential in Biospecimen Analysis and Outcome Prediction.Biomedicines · 2024Review
- MUC1-C Is a Common Driver of Acquired Osimertinib Resistance in NSCLC.Journal of thoracic oncology : official publication of the International Association for the Study of Lung Cancer · 2024Article
- Metabolic subtypes and immune landscapes in esophageal squamous cell carcinoma: prognostic implications and potential for personalized therapies.BMC cancer · 2024Article
- The multifaceted role of MUC1 in tumor therapy resistance.Clinical and experimental medicine · 2023Review
- Glycosylated modification of MUC1 maybe a new target to promote drug sensitivity and efficacy for breast cancer chemotherapy.Cell death & disease · 2022Article
- Addiction of Cancer Stem Cells to MUC1-C in Triple-Negative Breast Cancer Progression.International journal of molecular sciences · 2022Review
- The Wheat GeneFrontiers in plant science · 2022Article
- Mucin1 and Mucin16: Therapeutic Targets for Cancer Therapy.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Structure, regulation, and biological functions of TIGAR and its role in diseases.Acta pharmacologica Sinica · 2021Review
- LncRNA HCP5 promotes malignant cell behaviors in esophageal squamous cell carcinoma via the PI3K/AKT/mTOR signaling.Cell cycle (Georgetown, Tex.) · 2021Article
- Mucins reprogram stemness, metabolism and promote chemoresistance during cancer progression.Cancer metastasis reviews · 2021Review
- Review
- Targeting MUC1-C reverses the cisplatin resistance of esophageal squamous cell carcinomaTranslational cancer research · 2021Article
- Genetically Modified T Cells for Esophageal Cancer Therapy: A Promising Clinical Application.Frontiers in oncology · 2021Review
- Overexpression of Mucin 1 Suppresses the Therapeutical Efficacy of Disulfiram against Canine Mammary Tumor.Animals : an open access journal from MDPI · 2020Article
- Role of the MUC1-C oncoprotein in the acquisition of cisplatin resistance by urothelial carcinoma.Cancer science · 2020Article
- MUC1-C in chronic inflammation and carcinogenesis; emergence as a target for cancer treatment.Carcinogenesis · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Esophageal squamous cell carcinoma (ESCC) is one of the most common digestive tumors worldwide. The Mucin 1 (MUC1) heterodimeric protein has been confirmed that is overexpressed in ESCC and induced adverse outcomes. However, the detailed mechanism(s) remained challenging. So, we investigated the relationship between MUC1-C and metabolism in ESCC cells. In the results, TP53-induced glycolysis and apoptosis regulator (TIGAR) was overexpressed and correlative with MUC1-C positively in ESCC tissue. Targeting MUC1-C inhibits AKT-mTORC-S6K1 signaling and blocks TIGAR translation. We found that the inhibitory effect of GO-203 on TIGAR was mediated by inhibition of AKT-mTOR-S6K1 pathway. The findings also demonstrated that the suppressive effect of GO-203 on TIGAR is related to the decrease of glutathione level, the increase of reactive oxygen species and the loss of mitochondrial transmembrane membrane potential. In xenograft tissues, GO-203 inhibited the growth of ESCC cells and lead to the low expression of transmembrane C-terminal subunit (MUC1-C) and TIGAR. This evidence supports the contention that MUC1-C is significant for metabolism in ESCC and indicated that MUC1-C is a potential target for the treatment of ESCC.
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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.