ArticleTumor & microenvironment2021
Identification and Characterization of Glycine Decarboxylase as a Direct Target of Snail in the Epithelial-Mesenchymal Transition of Cancer Cells.
Article in Tumor & microenvironment, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- IL-21 isoform transgenic mice spontaneously develop mammary tumors: possible involvement of IL-21-induced osteopontin expression in tumorigenesis.Frontiers in immunology · 2026Article
- The Epithelial-Mesenchymal Transition at the Crossroads between Metabolism and Tumor Progression.International journal of molecular sciences · 2022Review
- Hormonal regulation of glycine decarboxylase and its relationship to oxidative stress.Physiological reports · 2021Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
CONTEXT/
aimsMetabolic reprogramming and cellular plasticity drive tumorigenesis. However, how these cellular events collectively contribute to the oncogenic process is poorly understood. Epithelial-mesenchymal transition (EMT), a fundamental mechanism of cellular plasticity, is governed by the EMT transcription repressors such as Snail. In the present study, through establishment and characterization of inducible overexpression of Snail in A549 lung cancer cells, we aim to define the metabolic reprogramming in response to Snail in the EMT of lung cancer cells. METHODS/
resultsOur metabolomic analysis suggests that forced expression of Snail accompanied reduced diversion of glycolytic metabolites to the serine/glycine metabolic shunt, a critical metabolic branch that distributes glucose catabolic intermediates to the major anabolic pathways. Our gene expression profiling and molecular characterization revealed that Snail actively suppressed the expression of glycine decarboxylase (GLDC), a key enzyme on the serine/glycine metabolic shunt, through binding to an evolutionarily conserved E-box motif and thereby inhibiting the promoter of the GLDC gene. Besides, knockdown of GLDC led to a cellular function shift from proliferation to migration.
conclusionThis study has revealed a novel molecular link that integrates the serine/glycine metabolism with the Snail-mediated EMT program in cancer cells.
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Registered trials
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