ArticleCell death & disease2024
TAB182 regulates glycolytic metabolism by controlling LDHA transcription to impact tumor radiosensitivity.
Article in Cell death & disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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The trial behind it
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Who cites it
11 citing papers in PubMed, 11 citations in OpenAlex.
- Crotonylation of ACAT1 K181 contributes to radioresistance by impacting lactate metabolism.Communications biology · 2026Article
- Lactylation enzymes in cancer: Mechanisms and novel therapeutic approaches (Review).Oncology letters · 2026Review
- Engineered Bacteria-Vesicle Delivered Lactate Reprogramming Boosts Tumor Radiosensitivity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Targeting Glycolytic Metabolism in Cancer Therapy: Current Approaches and Future Perspectives.Cells · 2026Review
- Tumor lactate metabolism shapes immune suppression and therapeutic resistance revealed by integrative multi-omics and digital pathology.Frontiers in immunology · 2026Article
- Review
- MicroRNA 195, lactate dehydrogenase 5, phosphatase and tensin homologue in colorectal cancer: Clinicopathology and prognosis.World journal of gastrointestinal surgery · 2025Article
- HBV DNA integration gene CCDC91 is oncogenic and a potential therapeutic target for hepatocellular carcinoma.Communications biology · 2025Article
- Lactate and lactylation in cancer.Signal transduction and targeted therapy · 2025Review
- Optimization of CAR-T therapy based on metabolic remodeling of the tumor immune microenvironment in diffuse large B-cell lymphoma.American journal of cancer research · 2025Review
- TNKS1BP1 facilitates ubiquitination of CNOT4 by TRIM21 to promote hepatocellular carcinoma progression and immune evasion.Cell death & disease · 2024Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metabolic reprogramming, a hallmark of cancer, is closely associated with tumor development and progression. Changes in glycolysis play a crucial role in conferring radiation resistance to tumor cells. How radiation changes the glycolysis status of cancer cells is still unclear. Here we revealed the role of TAB182 in regulating glycolysis and lactate production in cellular response to ionizing radiation. Irradiation can significantly stimulate the production of TAB182 protein, and inhibiting TAB182 increases cellular radiosensitivity. Proteomic analysis indicated that TAB182 influences several vital biological processes, including multiple metabolic pathways. Knockdown of TAB182 results in decreased lactate production and increased pyruvate and ATP levels in cancer cells. Moreover, knocking down TAB182 reverses radiation-induced metabolic changes, such as radioresistant-related lactate production. TAB182 is necessary for activating LDHA transcription by affecting transcription factors SP1 and c-MYC; its knockdown attenuates the upregulation of LDHA by radiation, subsequently suppressing lactate production. Targeted suppression of TAB182 significantly enhances the sensitivity of murine xenograft tumors to radiotherapy. These findings advance our understanding of glycolytic metabolism regulation in response to ionizing radiation, which may offer significant implications for developing new strategies to overcome tumor radioresistance.
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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 Socratic graph.