ArticleCancer cell international2023
ALKBH5-mediated CHAC1 depletion promotes malignant progression and decreases cisplatin-induced oxidative stress in gastric cancer.
Article in Cancer cell international, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 19 citations in OpenAlex.
- METTL16 S-glutathionylation-triggered RNA mActa pharmacologica Sinica · 2026Article
- Autophagy as a therapeutic target for cisplatin-resistant gastric cancer.Genes & diseases · 2026Review
- RNA modifications as determinants of cancer cell death: from epitranscriptomic mechanisms to therapeutic targeting.Functional & integrative genomics · 2026Review
- RNA mCell biology and toxicology · 2026Review
- A novel ferroptosis- and endoplasmic reticulum stress-related gene signature for predicting prognosis, immune features and drug sensitivity in gastric cancer.Discover oncology · 2026Article
- ALKBH5 inhibitors for cancer therapy: molecular docking, challenges and future prospects.Frontiers in pharmacology · 2026Review
- From Tumor Biology to Clinical Perspectives: Novel Biomarkers and Therapeutic Insights in Gastric Cancer.Oncology research · 2026Review
- Context-dependent functions of ALKBH5: a mechanistic framework linking cellular stress responses, immune regulation, viral infection, and therapeutic vulnerabilities.Frontiers in immunology · 2026Review
- Review
- CER1 as a manganese ion metabolism gene drives gastric cancer progression and therapeutic potential via oxidative stress and tumor microenvironment regulation.Discover oncology · 2025Article
- Mechanistic insights into the role of RNA demethylase ALKBH5 in malignant tumor therapy.Journal of translational medicine · 2025Review
- Oxidative Stress and Redox Signaling in Gastric Cancer: From Mechanisms to Therapeutic Implications.Antioxidants (Basel, Switzerland) · 2025Review
- Role of the mInternational journal of molecular medicine · 2025Review
- ALKBH5 suppresses gastric cancer tumorigenesis and metastasis by inhibiting the translation of uncapped WRAP53 RNA isoforms in an m6A-dependent manner.Molecular cancer · 2025Article
- CHAC1 in urological tumors: contextual dualism and therapeutic implications.Frontiers in oncology · 2025Review
- The strategic breakdown: CHAC enzymes as regulators of glutathione homeostasis and disease implications.Frontiers in molecular biosciences · 2025Review
- Role and mechanisms of m6A demethylases in digestive system tumors.American journal of cancer research · 2025Review
- Metformin enhances METTL14-Mediated m6A methylation to alleviate NIT-1 cells apoptosis induced by hydrogen peroxide.Heliyon · 2024Article
- CHAC1: a master regulator of oxidative stress and ferroptosis in human diseases and cancers.Frontiers in cell and developmental biology · 2024Review
- The Roles and Implications of m6A Methylation in Radiotherapy for Gastrointestinal Tumors.Dose-response : a publication of International Hormesis SocietyReview
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
The m6a demethyltransferase ALKBH5 dynamically modulates gene expression and intracellular metabolic molecules by modifying RNA m6a in cancer cells. However, ALKBH5's function in gastric cancer (GC) has remained controversial. This study demonstrates that ALKBH5 is highly expressed in GC. Silencing ALKBH5 hampers proliferation, and metastatic potential, and induces cell death in GC cells. Through a comprehensive analysis of the transcriptome and m6A sequencing, alterations in certain ALKBH5 target genes, including CHAC1, were identified. ALKBH5's demethylation effect regulates CHAC1 RNA stability, leading to reduced CHAC1 expression. Moreover, CHAC1 modulates intracellular ROS levels, influencing the chemotherapy sensitivity of gastric cancer. In summary, our study unveils the pivotal role of the ALKBH5-CHAC1-ROS axis and highlights the significance of m6A methylation in gastric cancer.
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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.