ArticleCancer cell international2024
Establishment of disulfidptosis-related LncRNA signature as biomarkers in colon adenocarcinoma.
Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- The emerging roles of disulfidptosis in cancer.Apoptosis : an international journal on programmed cell death · 2026Review
- PANX2 Suppresses Lung Adenocarcinoma Progression by Inducing Disulfidptosis and Enhancing Antitumor Immunity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Disulfidptosis vs. Ferroptosis: A Comprehensive Review of SLC7A11-Mediated Metal Dyshomeostasis and Cell Death.Biomolecules · 2026Review
- Disulfidptosis-Induced Chondrocyte-Macrophage Crosstalk via GYS1/CCND1/NOD2 Axis Promotes Osteoarthritis Progression.Journal of inflammation research · 2026Article
- Identification of disulfidptosis-related long non-coding RNA signature to predict the prognosis, immunotherapy, and chemotherapy options in acute myeloid leukemia.Translational cancer research · 2025Article
- Disulfide bond-related gene signature development for bladder cancer prognosis prediction and immune microenvironment characterization.Scientific reports · 2025Article
- CASC8 activates the pentose phosphate pathway to inhibit disulfidptosis in pancreatic ductal adenocarcinoma though the c-Myc-GLUT1 axis.Journal of experimental & clinical cancer research : CR · 2025Article
- Iron, copper and disulfide dysregulation: molecular crossroads of metabolic cell death in melanoma progression.Frontiers in pharmacology · 2025Review
- Multi‑cohort Validation Based on Disulfidptosis-Related lncRNAs for Predicting Prognosis and Immunotherapy Response of Esophageal Squamous Cell Carcinoma.OncoTargets and therapy · 2025Article
- Article
- TMEM105 modulates disulfidptosis and tumor growth in pancreatic cancer via the β-catenin-c-MYC-GLUT1 axis.International journal of biological sciences · 2025Article
- Stem cell status and prognostic applications of cuproptosis-associated lncRNAs in acute myeloid leukemia.Frontiers in cell and developmental biology · 2024Article
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4 authors.
Funding
Abstract
purposeMetabolic reprogramming is a hallmark of cancer and plays a key role in precision oncology treatment. Long non-coding RNAs (lncRNAs) regulate cancer cell behavior, including metabolism. Disulfidptosis, a newly identified form of regulated cell death triggered by glucose starvation, has yet to be fully understood in colon adenocarcinoma (COAD). This study aimed to confirm the existence and role of disulfidptosis in COAD and identify disulfidptosis-related lncRNAs that may be targeted to induce disulfidptosis in COAD.
methodsPI and F-actin staining were used to observe disulfidptosis in COAD cell lines. Disulfidptosis-related lncRNAs were identified based on the expression of disulfidptosis-associated genes in the TCGA-COAD database. A four-lncRNA signature for disulfidptosis was established. Subsequently, loss-of-function assays explored the roles of AC013652.1 and MCM3AP-AS1 in disulfidptosis.
resultsDisulfidptosis was observed in COAD cells under glucose starvation and could be reversed by agents that prevent disulfide stress, such as dithiothreitol (DTT) and tris-(2-carboxyethyl)-phosphine (TCEP). The prognostic value of disulfidptosis-associated genes in COAD patients was confirmed, with higher expression indicating longer survival. A disulfidptosis-related lncRNA signature comprising four lncRNAs was established based on the expression of these genes. Among these, AC013652.1 and MCM3AP-AS1 predicted worse prognoses. Furthermore, inhibiting AC013652.1 or MCM3AP-AS1 increased disulfidptosis-associated gene expression and cellular death, which could be reversed by DTT and TCEP.
conclusionsThis study provides hitherto undocumented evidence of the existence of disulfidptosis and the prognostic value of disulfidptosis-associated genes in COAD. Importantly, we identified lncRNAs AC013652.1 and MCM3AP-AS1, which suppress disulfidptosis and may serve as potential therapeutic targets for COAD.
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