ArticleScientific reports2024
ATF4 inhibits tumor development and mediates p-GCN2/ASNS upregulation in colon cancer.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- The stress-induced transcription factor ATF4 has multiple conserved retrocopies that can alter gene expression.HGG advances · 2026Article
- ATF4/SCO2 Inhibits Ferroptosis in Lung Cancer Through Activating the MAPK Signaling Pathway.Journal of biochemical and molecular toxicology · 2026Article
- PCBP1 orchestrates amino acid metabolism burst during the naïve-to-primed pluripotency transition.Stem cell reports · 2026Article
- MYC-ATF4-ASS1 axis governs intracellular arginine synthesis and dictates the immune microenvironment in melanoma.bioRxiv : the preprint server for biology · 2026Article
- Mechanisms of mTORC1 and GCN2 amino acid sensing pathways in tumorigenesis and metastatic progression (Review).International journal of molecular medicine · 2026Review
- Pinpointing an innovative autophagic signature as a prognostic and diagnostic biomarkers in colorectal carcinoma.Future science OA · 2025Article
- Emerging roles for integrated stress response signaling in homeostasis.The FEBS journal · 2025Review
- Amino acids in cancer: Understanding metabolic plasticity and divergence for better therapeutic approaches.Cell reports · 2025Review
- Canagliflozin differentially modulates carfilzomib-induced endoplasmic reticulum stress in multiple myeloma and endothelial cells.Archives of toxicology · 2025Article
- Crosstalk between dysregulated amino acid sensing and glucose and lipid metabolism in colorectal cancer.Frontiers in oncology · 2025Review
- A novel amphiphilic squalene-based compound with open-chain polyethers reduces malignant melanoma metastasis in-vitro and in-vivo.Cell communication and signaling : CCS · 2024Article
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4 authors.
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Abstract
Colon cancer (CC) is a highly malignant tumor with a high incidence and poor prognosis. This study aimed to explore the function and molecular mechanisms of activating transcription factor 4 (ATF4) in CC. The expression levels of ATF4, GCN2, and ASNS in CC tissues were measured using immunohistochemistry (IHC) and reverse transcription quantitative PCR (RT-qPCR). Cell counting kit-8 (CCK-8), clone formation, transwell, and flow cytometry assays were conducted to assess cell viability, clonogenicity, migration, invasion, cell cycle, and apoptosis, respectively, in the ATF4 knockdown and overexpression SW480 cell lines. The effect of ATF4 on the expression of GCN2 and ASNS was detected using RT-qPCR, Chip-qPCR, and western blotting. ATF4, GCN2, and ASNS were expressed at low levels in CC tissues, and all had a significant negative correlation with tumor diameter. ATF4 knockdown promoted cell proliferation, invasion, and S-phase cell cycle and inhibited apoptosis in SW480 cells. In contrast, ATF4 overexpression had the opposite effect. Furthermore, ATF4 overexpression enhanced ATF4 binding to the ASNS promoter region. ATF4 knockdown significantly inhibited the expression of p-GCN2 and ASNS, whereas ATF4 overexpression significantly upregulated their expression. ATF4 inhibited CC cell viability, clone formation ability, migration, and invasion and promoted apoptosis, possibly by regulating the expression of p-GCN2 and ASNS. Our study provides a novel potential therapeutic target for the treatment of CC.
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