ArticleAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2025
QSOX2-Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c-Myc Feedback Loop in Esophageal Squamous Cell Carcinoma.
Article in Advanced science (Weinheim, Baden-Wurttemberg, Germany), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The trial behind it
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Who cites it
8 citing papers in PubMed.
- The TBX18/SIX1 Transcriptional Circuit Maintains Stemness and EMT States to Promote Radioresistance in ESCC.Cancers · 2026Article
- Cancer drug response and resistance: molecular mechanisms and combating strategies.Signal transduction and targeted therapy · 2026Review
- Non-enzymatic function of QSOX2 directly regulates the JUNB-ITGB4 axis and enhanced resistance to osimertinib in EGFR-mutation lung adenocarcinoma.Cell death discovery · 2026Article
- Remodeling the tumor dormancy ecosystem to prevent recurrence and metastasis.Signal transduction and targeted therapy · 2026Review
- Hypoxia-Induced TGFBI Promotes Bladder Cancer Progression by Creating a Stemness Regulation Loop through Stabilizing the Disulfide Bonds of GDF15.Research (Washington, D.C.) · 2026Article
- Microenvironmental and Molecular Pathways Driving Dormancy Escape in Bone Metastases.International journal of molecular sciences · 2025Review
- QSOX2-Mediated Disulfide Bond Modification Enhances Tumor Stemness and Chemoresistance by Activating TSC2/mTOR/c-Myc Feedback Loop in Esophageal Squamous Cell Carcinoma.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- UBE2V1 Promotes Hepatocellular Carcinoma Progression by Forming a Positive Feedback Loop with HIF-1α.Research (Washington, D.C.) · 2025Article
Corrections and comments
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Authors and funding
13 authors.
Funding
Abstract
Disulfide bond modification is critical in maintaining protein structure and activity, but its roles in regulating tumor stemness and chemoresistance remain underexplored. Here, Quiescin Sulfhydryl Oxidase 2 (QSOX2) is identified, a protein involved in disulfide bond formation, is highly expressed in esophageal squamous cell carcinoma (ESCC), and is associated with poor patient prognosis. Functional analyses demonstrated that QSOX2 overexpression markedly potentiated tumor stemness and further promoted chemoresistance, proliferation, and metastasis of ESCC cells. Mechanistically, QSOX2 enhances disulfide bond formation in TSC Complex Subunit 2 (TSC2), stabilizing TSC2-Akt interactions, facilitating phosphorylation of TSC2 at the Ser939 by Akt, and further activating mTOR/4E-BP1/c-Myc signaling axis. Intriguingly, cancer-associated fibroblasts-secreted IGF-1 upregulates QSOX2 expression via IGF1R/Akt/mTOR/c-Myc pathway, establishing a positive feedback loop that sustains ESCC cell stemness. Targeting QSOX2 with Ebselen, in combination with mTOR inhibitor Rapamycin and chemotherapy, effectively downregulates c-Myc expression and induces tumor dormancy in a mouse xenograft model. Therefore, the findings reveal that QSOX2-mediated disulfide bond modification enhances tumor stemness by activating mTOR signaling, highlighting a promising therapeutic target in ESCC.
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