ArticleCancer communications (London, England)2022
PTPRO represses colorectal cancer tumorigenesis and progression by reprogramming fatty acid metabolism.
Article in Cancer communications (London, England), 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.
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Who cites it
71 citing papers in PubMed, 1 synthesis or guideline pooled it, 98 citations in OpenAlex.
- Current hotspots and trends in cancer metabolic reprogramming: a scientometric analysis.Frontiers in immunology · 2024Pooled it
- Metabolic reprogramming in colorectal cancer: Mechanisms and therapeutic insights.Genes & diseases · 2027Review
- Review
- RagC senses β-hydroxybutyrate abundancy to suppress mTORC1.Protein & cell · 2026Article
- Fatty Acid Metabolism and Hypoxia in the Tumor Microenvironment: Metabolic Adaptation and Clinical Potential in Colorectal Cancer.Biomedicines · 2026Review
- ACOT1-specific expression modulates metabolic reprogramming in diabetic cardiomyopathy: The role of SREBP1c lactylation in CD36-mediated lipotoxicity.American heart journal plus : cardiology research and practice · 2026Article
- IRX1 suppresses breast cancer progression by inhibiting fatty acid de novo synthesis through downregulating ACACA expression.Cell death & disease · 2026Article
- LRP2-mediated regulation of ferroptosis through the Wnt/β-catenin-GPX4 axis in colorectal cancer liver metastasis and chemoresistance.Cell death discovery · 2026Article
- Acetyl-CoA synthase 1 mediates metabolic reprogramming to promote proliferation and metastasis of osteosarcoma.Journal of orthopaedic translation · 2026Article
- The multifaceted roles of the ACSL family in cancer: Metabolic reprogramming, ferroptosis regulation and tumour immune microenvironment remodelling.Clinical and translational medicine · 2026Review
- RPS6KA1 Remodels Fatty Acid Metabolism and Suppresses Malignant Progression in Colorectal Cancer.Biomedicines · 2026Article
- PDK4-driven metabolic reprogramming enhances mesothelial cell invasion in colorectal cancer peritoneal metastasis.Acta biochimica et biophysica Sinica · 2026Article
- Fibroblast-derived POSTN promotes colorectal cancer progression under high-fat diet by reprogramming fatty acid metabolism in tumor cell.Cell communication and signaling : CCS · 2026Article
- Exploring the Relationship Between Colitis-Associated Cancer and Lipid Metabolism Reprogramming from the Perspective of Inflammation-Cancer Transformation.Journal of inflammation research · 2026Review
- FSCN1 Modulates Fatty Acid Metabolism and the Coordinated Activation of AKT/mTOR and p38 MAPK Pathways in Colorectal Cancer Cells.Oncology research · 2026Article
- Breast cancer cell-derived adrenomedullin confers cancer-associated adipose remodeling through the cAMP/Creb1/Zeb1 axis.British journal of cancer · 2025Article
- hnRNP A1 inhibits colorectal cancer tumorigenesis and progression by regulating fatty acid metabolism and RNA stability.Cell death discovery · 2025Article
- Review
- STING inhibits the progression of esophageal squamous cell carcinoma by suppressing CPT1A-mediated fatty acid β-oxidation.Acta pharmacologica Sinica · 2025Article
- Targeting Mitochondrial Cholesterol Efflux via TCF21/ABCA10 Pathway to Enhance Cisplatin Efficacy in Ovarian Cancer.Biochemical genetics · 2025Article
11 more citing papers are in PubMed but not listed here.
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12 authors at 2 institutions in 1 country.
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Abstract
backgroundAbnormal expression of protein tyrosine phosphatases (PTPs) has been reported to be a crucial cause of cancer. As a member of PTPs, protein tyrosine phosphatase receptor type O (PTPRO) has been revealed to play tumor suppressive roles in several cancers, while its roles in colorectal cancer (CRC) remains to be elucidated. Hence, we aimed to explore the roles and mechanisms of PTPRO in CRC initiation and progression.
methodsThe influences of PTPRO on the growth and liver metastasis of CRC cells and the expression patterns of different lipid metabolism enzymes were evaluated in vitro and in vivo. Molecular and biological experiments were conducted to uncover the underpinning mechanisms of dysregulated de novo lipogenesis and fatty acid β-oxidation.
resultsPTPRO expression was notably downregulated in CRC liver metastasis compared to the primary cancer, and such a downregulation was associated with poor prognosis of patients with CRC. PTPRO silencing significantly promoted cell growth and liver metastasis. Compared with PTPRO wild-type mice, PTPRO-knockout mice developed more tumors and harbored larger tumor loads under treatment with azoxymethane and dextran sulfate sodium. Gene set enrichment analysis revealed that PTPRO downregulation was significantly associated with the fatty acid metabolism pathways. Blockage of fatty acid synthesis abrogated the effects of PTPRO silencing on cell growth and liver metastasis. Further experiments indicated that PTPRO silencing induced the activation of the AKT serine/threonine kinase (AKT)/mammalian target of rapamycin (mTOR) signaling axis, thus promoting de novo lipogenesis by enhancing the expression of sterol regulatory element-binding protein 1 (SREBP1) and its target lipogenic enzyme acetyl-CoA carboxylase alpha (ACC1) by activating the AKT/mTOR signaling pathway. Furthermore, PTPRO attenuation decreased the fatty acid oxidation rate by repressing the expression of peroxisome proliferator-activated receptor alpha (PPARα) and its downstream enzyme peroxisomal acyl-coenzyme A oxidase 1 (ACOX1) via activating the p38/extracellular signal-regulated kinase (ERK) mitogen-activated protein kinase (MAPK) signaling pathway.
conclusionsPTPRO could suppress CRC development and metastasis via modulating the AKT/mTOR/SREBP1/ACC1 and MAPK/PPARα/ACOX1 pathways and reprogramming lipid metabolism.
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