ArticleOncotarget2017
Glucose deprivation elicits phenotypic plasticity via ZEB1-mediated expression of NNMT.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed.
- Nicotinamide N-methyltransferase as a therapeutic target in taxane-resistant castration-resistant prostate cancer.Cell death discovery · 2026Article
- Molecular and cellular landscapes of the immune microenvironment and multiomic biomarker-sets in platinum-resistant recurrent ovarian cancers.Journal of ovarian research · 2026Review
- Nicotinamide N-methyltransferase gene silencing is associated with upregulation of X-inactive specific transcript and downregulation of stemness-related transcription factors in ovarian cancer.Molecular biology reports · 2026Article
- Exploring NNMT: from metabolic pathways to therapeutic targets.Archives of pharmacal research · 2024Review
- Biological Functions and Therapeutic Potential of NADCancers · 2024Review
- NNMT overexpression is an adverse prognostic factor in uterine leiomyosarcoma.Turkish journal of medical sciences · 2024Article
- Real-time redox adaptations in human airway epithelial cells exposed to isoprene hydroxy hydroperoxide.Redox biology · 2023Article
- The crosstalk among the physical tumor microenvironment and the effects of glucose deprivation on tumors in the past decade.Frontiers in cell and developmental biology · 2023Review
- A comprehensive overview of recent developments on the mechanisms and pathways of ferroptosis in cancer: the potential implications for therapeutic strategies in ovarian cancer.Cancer drug resistance (Alhambra, Calif.) · 2023Review
- NicotinamideACS omega · 2022Article
- Nicotinamide-N-methyltransferase is a promising metabolic drug target for primary and metastatic clear cell renal cell carcinoma.Clinical and translational medicine · 2022Article
- Complex roles of nicotinamide N-methyltransferase in cancer progression.Cell death & disease · 2022Review
- Nicotinamide N-Methyltransferase: A Promising Biomarker and Target for Human Cancer Therapy.Frontiers in oncology · 2022Review
- Methylosystem for Cancer Sieging Strategy.Cancers · 2021Review
- Nicotinamide N-Methyltransferase in Acquisition of Stem Cell Properties and Therapy Resistance in Cancer.International journal of molecular sciences · 2021Review
- Patients with low nicotinamide N-methyltransferase expression benefit significantly from bevacizumab treatment in ovarian cancer.BMC cancer · 2021Article
- Expression of Ferroptosis-Related Genes Shapes Tumor Microenvironment and Pharmacological Profile in Gastric Cancer.Frontiers in cell and developmental biology · 2021Article
- Overexpression of Nicotinamide N-methyltransferase mainly covers stroma of colorectal cancer and correlates with unfavorable survival by its product 1-MNA.Journal of Cancer · 2021Article
- Implementing Curcumin in Translational Oncology Research.Molecules (Basel, Switzerland) · 2020Review
- Identification of two microRNA nodes as potential cooperative modulators of liver metabolism.Hepatology research : the official journal of the Japan Society of Hepatology · 2019Article
Corrections and comments
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Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose is considered the primary energy source for all cells, and some cancers are addicted to glucose. Here, we investigated the functional consequences of chronic glucose deprivation in serous ovarian cancer cells. We found that cells resistant to glucose starvation (glucose-restricted cells) demonstrated increased metabolic plasticity that was dependent on NNMT (Nicotinamide N-methyltransferase) expression. We further show that ZEB1 induced NNMT, rendered cells resistant to glucose deprivation and recapitulated metabolic adaptations and mesenchymal gene expression observed in glucose-restricted cells. NNMT depletion reversed metabolic plasticity in glucose-restricted cells and prevented de novo formation of glucose-restricted colonies. In addition to its role in glucose independence, we found that NNMT was required for other ZEB1-induced phenotypes, such as increased migration. NNMT protein levels were also elevated in metastatic and recurrent tumors compared to matched primary carcinomas, while normal ovary and fallopian tube tissue had no detectable NNMT expression. Our studies define a novel ZEB1/NNMT signaling axis, which elicits mesenchymal gene expression, as well as phenotypic and metabolic plasticity in ovarian cancer cells upon chronic glucose starvation. Understanding the causes of cancer cell plasticity is crucial for the development of therapeutic strategies to counter intratumoral heterogeneity, acquired drug resistance and recurrence in high-grade serous ovarian cancer (HGSC).
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