ArticleOncogene2018
CAB39L elicited an anti-Warburg effect via a LKB1-AMPK-PGC1α axis to inhibit gastric tumorigenesis.
Article in Oncogene, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers, 3 of them syntheses that pooled it.
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Who cites it
45 citing papers in PubMed, 3 syntheses or guidelines pooled it, 69 citations in OpenAlex.
- Integrative functional bioinformatic analysis of NADFrontiers in endocrinology · 2026Pooled it
- Association of Genetic Variant at Chromosome 12q23.1 With Neuropathic Pain Susceptibility.JAMA network open · 2021Pooled it
- Do polymorphisms in protein kinase catalytic subunit alpha-1 gene associated with cancer susceptibility? a meta-analysis and systematic review.BMC medical genetics · 2018Pooled it
- Prostaglandin ETheranostics · 2019Trial
- Bone matrix-inspired whitlockite porous ceramic with effects of autophagy activation contributes to bone regeneration.Bioactive materials · 2026Article
- Association ofTranslational cancer research · 2026Article
- Identification of an m7G-Related lncRNA Signature for Prognostic Prediction and Immune Landscape Characterization in Early Gastric Cancer.OncoTargets and therapy · 2026Article
- RNA mCancer communications (London, England) · 2025Article
- CRISPR-RfxCas13d screening uncovers Bckdk as a post-translational regulator of maternal-to-zygotic transition in teleosts.The EMBO journal · 2025Article
- miR-3662 targets CAB39L to promote proliferation and invasion in gastric cancer.Clinical and experimental medicine · 2025Article
- Article
- High-grade corded and hyalinized endometrioid carcinoma with high microsatellite instability and STK11 mutation: A case report and literature review.Oncology letters · 2025Article
- Insights into targeting LKB1 in tumorigenesis.Genes & diseases · 2025Review
- The role of mitochondrial biogenesis, mitochondrial dynamics and mitophagy in gastrointestinal tumors.Cancer cell international · 2025Review
- LKB1 inactivation promotes epigenetic remodeling-induced lineage plasticity and antiandrogen resistance in prostate cancer.Cell research · 2025Article
- Weitiao No. 3 (3) enhances the efficacy of anti-programmed cell death protein-1 immunotherapy by modulating the intestinal microbiota in an orthotopic model of gastric cancer mice.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2024Article
- Steatotic liver disease induced by TCPOBOP-activated hepatic constitutive androstane receptor: primary and secondary gene responses with links to disease progression.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Review
- Loss of LPAR6 and CAB39L dysregulates the basal-to-luminal urothelial differentiation program, contributing to bladder carcinogenesis.Cell reports · 2024Article
- RNA Expression of MMP12 Is Strongly Associated with Inflammatory Bowel Disease and Is Regulated by Metabolic Pathways in RAW 264.7 Macrophages.International journal of molecular sciences · 2024Article
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
Abstract
Metabolic dysfunction is a hallmark of gastric cancer (GC). In this study, we reported the identification of Calcium Binding Protein 39-Like (CAB39L) as a novel regulator of tumor metabolism in GC. CAB39L mRNA was frequently silenced by promoter methylation in GC cell lines and tissues. Functional studies suggested that CAB39L functions as a tumor suppressor, as overexpression of CAB39L elicited suppression of multiple cancer phenotypes both in GC cells and an orthotopic mouse model; whilst its knockdown promoted tumorigenesis. Mechanistically, CAB39L interacted with LKB1-STRAD complex and induced LKB1, leading to the phosphorylation and activation of AMPKα/β. LKB1-AMPK activation in GC cell lines was tumor suppressive, as metformin (an AMPK activator) inhibited GC cell growth in the CAB39L-silenced cells. Moreover, knockdown of LKB1 reversed growth inhibitory effect of CAB39L, indicating that tumor suppression by CAB39L depended on LKB1-AMPK. RNAseq and gene set enrichment analysis revealed that CAB39L was closely correlated with oxidative phosphorylation and mitochondrial biogenesis. Consistently, CAB39L-induced p-AMPK elicited PGC1α phosphorylation and increased the expression of genes involved in mitochondrial respiration complexes. Accordingly, CAB39L reversed the Warburg effect in GC, as evidenced by enhanced oxygen consumption rate and reduced extracellular acidification rate; inversely, CAB39L knockdown promoted a metabolic shift towards the Warburg phenotype. In GC patients, CAB39L promoter hypermethylation was correlated with poor prognosis. Our data demonstrate that CAB39L is a novel tumor suppressor which suppresses tumorigenesis by promoting LKB1-AMPK-PGC1α axis, thereby preventing a metabolic shift that drives carcinogenesis. CAB39L methylation is a potential prognostic biomarker for GC patients.
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