ArticleBMC cancer2012
Carnitine palmitoyltransferase 1A (CPT1A): a transcriptional target of PAX3-FKHR and mediates PAX3-FKHR-dependent motility in alveolar rhabdomyosarcoma cells.
Article in BMC cancer, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- Trial
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- Inhibition of lipid metabolism exerts antitumor effects on rhabdomyosarcoma.Cancer medicine · 2021Article
- Nanotechnology-Based Strategies to Evaluate and Counteract Cancer Metastasis and Neoangiogenesis.Advanced healthcare materials · 2021Review
- ACTA1 is inhibited by PAX3-FOXO1 through RhoA-MKL1-SRF signaling pathway and impairs cell proliferation, migration and tumor growth in Alveolar Rhabdomyosarcoma.Cell & bioscience · 2021Article
- Characterization of mTOR Activity and Metabolic Profile in Pediatric Rhabdomyosarcoma.Cancers · 2020Article
- Targeting the undruggable: exploiting neomorphic features of fusion oncoproteins in childhood sarcomas for innovative therapies.Cancer metastasis reviews · 2019Review
- Therapeutic Approaches Targeting PAX3-FOXO1 and Its Regulatory and Transcriptional Pathways in Rhabdomyosarcoma.Molecules (Basel, Switzerland) · 2018Review
- Lipid metabolism and lipophagy in cancer.Biochemical and biophysical research communications · 2018Review
- HNRNPH1 is required for rhabdomyosarcoma cell growth and survival.Oncogenesis · 2018Article
- Downregulation of CPT2 promotes tumorigenesis and chemoresistance to cisplatin in hepatocellular carcinoma.OncoTargets and therapy · 2018Article
- Metformin induces cell cycle arrest at the G1 phase through E2F8 suppression in lung cancer cells.Oncotarget · 2017Article
- SPA70 is a potent antagonist of human pregnane X receptor.Nature communications · 2017Article
- Transcription factor ZNF148 is a negative regulator of human muscle differentiation.Scientific reports · 2017Article
- Mesenchymal Stem Cells Induce Epithelial to Mesenchymal Transition in Colon Cancer Cells through Direct Cell-to-Cell Contact.Neoplasia (New York, N.Y.) · 2017Article
- The RhoE/ROCK/ARHGAP25 signaling pathway controls cell invasion by inhibition of Rac activity.Molecular biology of the cell · 2016Article
- Fatty acid oxidation and carnitine palmitoyltransferase I: emerging therapeutic targets in cancer.Cell death & disease · 2016Review
- Methods to Study Mrp4-containing Macromolecular Complexes in the Regulation of Fibroblast Migration.Journal of visualized experiments : JoVE · 2016Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAlveolar rhabdomyosarcoma (ARMS) has a high propensity to metastasize, leading to its aggressiveness and a poor survival rate among those with the disease. More than 80% of aggressive ARMSs harbor a PAX3-FKHR fusion transcription factor, which regulates cell migration and promotes metastasis, most likely by regulating the fusion protein's transcriptional targets. Therefore, identifying druggable transcription targets of PAX3-FKHR that are also downstream effectors of PAX3-FKHR-mediated cell migration and metastasis may lead to novel therapeutic approaches for treating ARMS.
methodsTo identify genes whose expression is directly affected by the level of PAX3-FKHR in an ARMS cellular-context, we first developed an ARMS cell line in which PAX3-FKHR is stably down-regulated, and showed that stably downregulating PAX3-FKHR in ARMS cells significantly decreased the cells' motility. We used microarray analysis to identify genes whose expression level decreased when PAX3-FKHR was downregulated. We used mutational analysis, promoter reporter assays, and electrophoretic mobility shift assays to determine whether PAX3-FKHR binds to the promoter region of the target gene. We used siRNA and pharmacologic inhibitor to downregulate the target gene of PAX3-FKHR and investigated the effect of such downregulation on cell motility.
resultsWe found that when PAX3-FKHR was downregulated, the expression of carnitine palmitoyltransferase 1A (CPT1A) decreased. We showed that PAX3-FKHR binds to a paired-domain binding-site in the CPT1A promoter region, indicating that CPT1A is a novel transcriptional target of PAX3-FKHR. Furthermore, downregulating CPT1A decreased cell motility in ARMS cells, indicating that CPT1A is a downstream effector of PAX3-FKHR-mediated cell migration and metastasis.
conclusionsTaken together, we have identified CPT1A as a novel transcriptional target of PAX3-FKHR and revealed the novel function of CPT1A in promoting cell motility. CPT1A may represent a novel therapeutic target for the treatment of ARMS.
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