ArticleOncotarget2015
Deciphering the molecular basis of invasiveness in Sdhb-deficient cells.
Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 66 citations in OpenAlex.
- Case Report: The silent giant: biochemical-clinical dissociation in a large cystic pheochromocytoma.Frontiers in oncology · 2026Article
- The impact of epithelial-mesenchymal transition (EMT) induced by metabolic processes and intracellular signaling pathways on chemo-resistance, metastasis, and recurrence in solid tumors.Cell communication and signaling : CCS · 2024Review
- The role of methylation quantification of circulating tumor DNA (ctDNA) as a diagnostic biomarker of Pheochromocytomas (PCCs) and Paragangliomas (PGLs).Journal of diabetes and metabolic disorders · 2024Article
- Genomic and immune landscape Of metastatic pheochromocytoma and paraganglioma.Nature communications · 2023Article
- Hereditary Endocrine Tumor Registries.Journal of the Endocrine Society · 2023Article
- Tumour microenvironment in pheochromocytoma and paraganglioma.Frontiers in endocrinology · 2023Review
- Metformin Treatment Induces Different Response in Pheochromocytoma/Paraganglioma Tumour Cells and in Primary Fibroblasts.Cancers · 2022Article
- Loss of SDHB Induces a Metabolic Switch in the hPheo1 Cell Line toward Enhanced OXPHOS.International journal of molecular sciences · 2022Article
- MicroRNA-96: A therapeutic and diagnostic tumor marker.Iranian journal of basic medical sciences · 2022Review
- Establishment of Patient-Derived Succinate Dehydrogenase-Deficient Gastrointestinal Stromal Tumor Models for Predicting Therapeutic Response.Clinical cancer research : an official journal of the American Association for Cancer Research · 2022Article
- Model systems in SDHx-related pheochromocytoma/paraganglioma.Cancer metastasis reviews · 2021Review
- Loss of SDHB Promotes Dysregulated Iron Homeostasis, Oxidative Stress, and Sensitivity to Ascorbate.Cancer research · 2021Article
- From Metabolism to Genetics and Vice Versa: The Rising Role of Oncometabolites in Cancer Development and Therapy.International journal of molecular sciences · 2021Review
- Targeting Mitochondrial Oncometabolites: A New Approach to Overcome Drug Resistance in Cancer.Pharmaceutics · 2021Review
- Interplay between Metabolism Reprogramming and Epithelial-to-Mesenchymal Transition in Cancer Stem Cells.Cancers · 2021Review
- Review
- Mutation of the Cell Cycle Regulator p27kip1 Drives Pseudohypoxic Pheochromocytoma Development.Cancers · 2021Article
- The Crucial Roles of Intermediate Metabolites in Cancer.Cancer management and research · 2021Review
- Integrative Analysis of Metabolomics and Transcriptomics Data Identifies Prognostic Biomarkers Associated With Oral Squamous Cell Carcinoma.Frontiers in oncology · 2021Article
- Pyruvate Dehydrogenase Contributes to Drug Resistance of Lung Cancer Cells Through Epithelial Mesenchymal Transition.Frontiers in cell and developmental biology · 2021Article
Corrections and comments
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Authors and funding
13 authors at 9 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Metastatic pheochromocytomas and paragangliomas (PPGL) are malignant neuroendocrine tumors frequently associated with germline mutations in the SDHB gene. SDHB-mutated PPGL display a hypermethylator phenotype associated with hallmarks of epithelial-to-mesenchymal transition (EMT). In the present study, we report the characterization of a unique model of Sdhb knockout in mouse chromaffin cells. Sdhb deficient cells exhibit a metastatic phenotype as highlighted by increased individual cell migration (characterized by faster motility and increased persistence) as well as high invasive and adhesion abilities. This phenotype is associated with the modulation of Twist1, Twist2, Tcf3, Snai1, N-cadherin or Krt19 expression, reflecting an EMT-like reprogramming of cells. Krt19 is epigenetically silenced in Sdhb-deficient cells and re-expressed after treatment by the demethylating agent decitabine. Krt19 rescue by lentiviral transduction in Sdhb-deficient cells and Krt19 inhibition by RNA interference in wild-type cells were performed. Both studies revealed the involvement of KRT19 in the invasive phenotype by modulating collective and individual migration and cell/extra-cellular matrix adhesion properties. These findings underline the role of hypermethylation and EMT in the in vitro acquisition of metastatic properties, following SDHB loss of function.
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