ArticleEndocrine-related cancer2019
ATM deficiency promotes progression of CRPC by enhancing Warburg effect.
Article in Endocrine-related cancer, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
19 citing papers in PubMed, 36 citations in OpenAlex.
- Targeting the Warburg Effect in Anaplastic Thyroid Carcinoma: Metabolic Vulnerabilities and Therapeutic Opportunities.International journal of molecular sciences · 2026Review
- Single-cell analysis revealing the metabolic landscape of prostate cancer.Asian journal of andrology · 2024Article
- Review
- A novel targeted NGS panel identifies numerous homologous recombination deficiency (HRD)-associated gene mutations in addition to known BRCA mutations.Diagnostic pathology · 2024Article
- Lactate as Key Metabolite in Prostate Cancer Progression: What Are the Clinical Implications?Cancers · 2023Review
- Metabolic changes during prostate cancer development and progression.Journal of cancer research and clinical oncology · 2023Review
- Glycine Decarboxylase (GLDC) Plays a Crucial Role in Regulating Energy Metabolism, Invasion, Metastasis and Immune Escape for Prostate Cancer.International journal of biological sciences · 2023Article
- Androgen Receptor Splice Variants Contribute to the Upregulation of DNA Repair in Prostate Cancer.Cancers · 2022Article
- An anaplerotic approach to correct the mitochondrial dysfunction in ataxia-telangiectasia (A-T).Molecular metabolism · 2021Article
- Article
- ELOVL5-Mediated Long Chain Fatty Acid Elongation Contributes to Enzalutamide Resistance of Prostate Cancer.Cancers · 2021Article
- Allele-Specific MicroRNA-Mediated Regulation of a Glycolysis Gatekeeper PDK1 in Cancer Metabolism.Cancers · 2021Article
- A glutaminase isoform switch drives therapeutic resistance and disease progression of prostate cancer.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Metabolic reprogramming as an emerging mechanism of resistance to endocrine therapies in prostate cancer.Cancer drug resistance (Alhambra, Calif.) · 2021Review
- O-GlcNAcylation in Chronic Lymphocytic Leukemia and Other Blood Cancers.Frontiers in immunology · 2021Review
- Poly(ADP-Ribose) Polymerase Inhibitors in Prostate Cancer: Molecular Mechanisms, and Preclinical and Clinical Data.Targeted oncology · 2020Review
- Article
- MicroRNA-488 inhibits proliferation and glycolysis in human prostate cancer cells by regulating PFKFB3.FEBS open bio · 2019Article
- Identifying the role of apolipoprotein A-I in prostate cancer.Asian journal of andrologyArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
ATM is a well-known master regulator of double strand break (DSB) DNA repair and the defective DNA repair has been therapeutically exploited to develop PARP inhibitors based on the synthetic lethality strategy. ATM mutation is found with increased prevalence in advanced metastatic castration-resistant prostate cancer (mCRPC). However, the molecular mechanisms underlying ATM mutation-driving disease progression are still largely unknown. Here, we report that ATM mutation contributes to the CRPC progression through a metabolic rather than DNA repair mechanism. We showed that ATM deficiency generated by CRISPR/Cas9 editing promoted CRPC cell proliferation and xenograft tumor growth. ATM deficiency altered cellular metabolism and enhanced Warburg effect in CRPC cells. We demonstrated that ATM deficiency shunted the glucose flux to aerobic glycolysis by upregulating LDHA expression, which generated more lactate and produced less mitochondrial ROS to promote CRPC cell growth. Inhibition of LDHA by siRNA or inhibitor FX11 generated less lactate and accumulated more ROS in ATM-deficient CRPC cells and therefore potentiated the cell death of ATM-deficient CRPC cells. These findings suggest a new therapeutic strategy for ATM-mutant CRPC patients by targeting LDHA-mediated glycolysis metabolism, which might be effective for the PARP inhibitor resistant mCRPC tumors.
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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.