ArticleOncoTargets and therapy2021
Targeting the IDO-BCL2A1-Cytochrome c Pathway Promotes Apoptosis in Oral Squamous Cell Carcinoma.
Article in OncoTargets and therapy, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 15 citations in OpenAlex.
- HCellular & molecular biology letters · 2026Article
- 3-Hydroxyanthranic acid inhibits growth of oral squamous carcinoma cells through growth arrest and DNA damage inducible alpha.Translational oncology · 2025Article
- Low Indoleamine 2,3-Dioxygenase 1 Expression Enhances Dendritic Cells Response to Tumor Cells Against Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2025Article
- Reconstructing oral cavity tumor evolution through brush biopsy.Scientific reports · 2024Article
- Article
- ADAR1 Inhibits Macrophage Apoptosis and Alleviates Sepsis-induced Liver Injury Through miR-122/BCL2A1 Signaling.Journal of clinical and translational hepatology · 2024Article
- Assessment of an Anticancer Effect of the Simultaneous Administration of MM-129 and Indoximod in the Colorectal Cancer Model.Cancers · 2023Article
- The cross-talk between macrophages and tumor cells as a target for cancer treatment.Frontiers in oncology · 2023Review
- Untargeted metabolomics analysis reveals Mycobacterium tuberculosis strain H37Rv specifically induces tryptophan metabolism in human macrophages.BMC microbiology · 2022Article
- Therapeutic targets and biomarkers of tumor immunotherapy: response versus non-response.Signal transduction and targeted therapy · 2022Review
- [Research Progress in the Association between Amino Acid Metabolism of Oral Microorganisms and Host Cells and Oral Diseases].Sichuan da xue xue bao. Yi xue ban = Journal of Sichuan University. Medical science edition · 2022Review
- Proliferation and Apoptosis Pathways and Factors in Oral Squamous Cell Carcinoma.International journal of molecular sciences · 2022Review
- Circulating Natural Autoantibodies to HER2-Derived Peptides Performed Antitumor Effects on Oral Squamous Cell Carcinoma.Frontiers in pharmacology · 2021Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeIndolamine 2,3-dioxygenase (IDO) is the rate limiting enzyme of tryptophan degradation and is a negative prognostic factor in oral squamous cell carcinoma (OSCC) patients, while the underlying molecular mechanism remains unclear. This research aimed to explore the IDO expression and its biological functions in OSCC. MATERIALS AND
methodsIDO expression was analyzed by qPCR, Western blots, and immunohistochemistry (IHC) in OSCC cell lines and tissue specimens. Tryptophan and kynurenine content were determined by UPLC-MS/MS in serum samples of OSCC patients and healthy controls. Oncomine databases and Kaplan-Meier survival analyses were used to identify the IDO expression and its correlation with OSCC prognosis. Cell counting, CCK8 assay, flow cytometry, cell cycle, and EdU incorporation assays were used to assess the effect of IDO inhibition on OSCC growth either by shRNA or the IDO-specific inhibitor (epacadostat) in vitro. An OSCC xenograft mouse model was established to verify the predicted function of IDO inhibition in vivo. Mechanistically, an 84-gene apoptosis PCR array and rescue experiment were used to characterize the underlying mechanism involved in IDO-regulated apoptosis in OSCC.
resultsIDO expression was upregulated in OSCC cell lines and tissues and was negatively correlated with OSCC progression. Lentivirus-mediated IDO knockdown and epacadostat significantly reduced viability and promoted apoptosis of OSCC cells in vitro and in vivo. The apoptosis PCR array identified BCL2 related protein A1 (BCL2A1) as the most obviously changed gene at the transcriptional level. IDO inhibition downregulated BCL2A1 expression, increased the expression and translocation of cytochrome c, thus promoted apoptosis in OSCC. Overexpression of BCL2A1 reversed the pro-apoptotic effect of IDO inhibition.
conclusionThe present results revealed that IDO directly affect the growth of OSCC cells by regulating BCL2A1 expression. IDO and the IDO-BCL2A1-cytochrome c axis may be potential therapeutic targets for OSCC.
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