ArticleCarcinogenesis2010
NSAID-activated gene-1 as a molecular target for capsaicin-induced apoptosis through a novel molecular mechanism involving GSK3beta, C/EBPbeta and ATF3.
Article in Carcinogenesis, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.
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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
45 citing papers in PubMed, 101 citations in OpenAlex.
- Arteannuin B Induces Ferroptosis in Colorectal Cancer Cells via GDF15/HMGCS1/GPX4 Axis.Journal of Cancer · 2026Article
- Quercetin and microRNA Interplay in Apoptosis Regulation: A New Therapeutic Strategy for Cancer?Current medicinal chemistry · 2025Review
- Hepatocyte-specific GDF15 overexpression improves high-fat diet-induced obesity and hepatic steatosis in mice via hepatic FGF21 induction.Scientific reports · 2024Article
- Macrophages as a Source and Target of GDF-15.International journal of molecular sciences · 2024Review
- Molecular basis of GDF15 induction and suppression by drugs in cardiomyocytes and cancer cells toward precision medicine.Scientific reports · 2023Article
- Natural Polyphenols for Treatment of Colorectal Cancer.Molecules (Basel, Switzerland) · 2022Review
- Biomedical and Antioxidant Potentialities in Chilli: Perspectives and Way Forward.Molecules (Basel, Switzerland) · 2022Review
- Local anesthetic lidocaine-inducible gene, growth differentiation factor-15 suppresses the growth of cancer cell lines.Scientific reports · 2022Article
- Deletion of Gdf15 Reduces ER Stress-induced Beta-cell Apoptosis and Diabetes.Endocrinology · 2022Article
- Emerging role of natural products in cancer immunotherapy.Acta pharmaceutica Sinica. B · 2022Review
- Mechanism of sensitivity to cisplatin, docetaxel, and 5-fluorouracil chemoagents and potential erbB2 alternatives in oral cancer with growth differentiation factor 15 overexpression.Cancer science · 2022Article
- The Antifibrotic and the Anticarcinogenic Activity of Capsaicin in Hot Chili Pepper in Relation to Oral Submucous Fibrosis.Frontiers in pharmacology · 2022Review
- Anticancer Effect of Spices Used in Mediterranean Diet: Preventive and Therapeutic Potentials.Frontiers in nutrition · 2022Review
- ATF3 promotes the serine synthesis pathway and tumor growth under dietary serine restriction.Cell reports · 2021Article
- Quercetin Induces Anticancer Activity by Upregulating Pro-NAG-1/GDF15 in Differentiated Thyroid Cancer Cells.Cancers · 2021Article
- Natural Products in the Prevention of Metabolic Diseases: Lessons Learned from the 20th KAST Frontier Scientists Workshop.Nutrients · 2021Review
- Glucocorticoids ElevateFrontiers in microbiology · 2021Article
- Quercetin as an innovative therapeutic tool for cancer chemoprevention: Molecular mechanisms and implications in human health.Cancer medicine · 2020Review
- GDF15: A Hormone Conveying Somatic Distress to the Brain.Endocrine reviews · 2020Review
- Effects of non-steroidal anti-inflammatory drug-activated gene-1 on Ganoderma lucidum polysaccharides-induced apoptosis of human prostate cancer PC-3 cells.International journal of oncology · 2018Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Capsaicin, a natural product of the Capsicum species of red peppers, is known to induce apoptosis and suppress growth. Non-steroidal anti-inflammatory drug-activated gene-1 (NAG-1) is a cytokine associated with pro-apoptotic and antitumorigenic property in colorectal and lung cancer. Our data demonstrate that capsaicin leads to induction of apoptosis and up-regulates NAG-1 gene expression at the transcriptional level. Overexpression of CCAAT/enhancer binding protein beta (C/EBPbeta) caused a significant increase of basal and capsaicin-induced NAG-1 promoter activity. We subsequently identified C/EBPbeta binding sites in the NAG-1 promoter responsible for capsaicin-induced NAG-1 transactivation. Electrophoretic mobility shift assay and chromatin immunoprecipitation assay confirmed binding of C/EBPbeta to the NAG-1 promoter. Capsaicin treatment resulted in an increase of phosphorylated serine/threonine residues on C/EBPbeta, and the immunoprecipitation study showed that capsaicin enhanced binding of C/EBPbeta with glycogen synthase kinase 3beta (GSK3beta) and activating transcription factor 3 (ATF3). The phosphorylation and interaction of C/EBPbeta with GSK3beta and ATF3 are decreased by the inhibition of the GSK3beta and Protein Kinase C pathways. Knockdown of C/EBPbeta, GSK3beta or ATF3 ameliorates NAG-1 expression induced by capsaicin treatment. These data indicate that C/EBPbeta phosphorylation through GSK3beta may mediate capsaicin-induced expression of NAG-1 and apoptosis through cooperation with ATF3 in human colorectal cancer cells.
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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.