ArticleCell death & disease2017
Loss of the novel mitochondrial protein FAM210B promotes metastasis via PDK4-dependent metabolic reprogramming.
Article in Cell death & disease, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 62 citations in OpenAlex.
- Comprehensive analysis of metabolic reprogramming-related gene signatures for predicting ovarian cancer prognosis, the immune landscape, and potential treatment options.Discover oncology · 2026Article
- FAM210B regulates iron homeostasis and sex-specific responses in stress erythropoiesis.Experimental hematology · 2025Article
- The impact of ERCell death & disease · 2025Article
- FAM210B Regulates Iron Homeostasis and Sex-Specific Responses in Stress Erythropoiesis.bioRxiv : the preprint server for biology · 2025Article
- FAM210B activates STAT1/IRF9/IFIT3 axis by upregulating IFN-α/β expression to impede the progression of lung adenocarcinoma.Cell death & disease · 2025Article
- Multifaceted role of FAM210B in hepatocellular carcinoma: Implications for tumour progression, microenvironment modulation and therapeutic selection.Journal of cellular and molecular medicine · 2024Article
- Deletion of the Mitochondrial Membrane Protein Fam210b Is Associated with the Development of Systemic Lupus Erythematosus.International journal of molecular sciences · 2024Article
- Pan-cancer analysis reveals PDK family as potential indicators related to prognosis and immune infiltration.Scientific reports · 2024Article
- PDK4-dependent hypercatabolism and lactate production of senescent cells promotes cancer malignancy.Nature metabolism · 2023Article
- Targeting Aggressive B-cell Lymphomas through Pharmacological Activation of the Mitochondrial Protease OMA1.Molecular cancer therapeutics · 2023Article
- Article
- Promotive role of eukaryotic translation initiation factor 4A isoform 3 in ovarian cancer cell growth and aerobic glycolysis through the pyruvate dehydrogenase kinase 4 signaling.The Kaohsiung journal of medical sciences · 2023Article
- Loss of the Novel Mitochondrial Membrane Protein FAM210B Is Associated with Hepatocellular Carcinoma.Biomedicines · 2023Article
- Elucidation of the Role of FAM210B in Mitochondrial Metabolism and Erythropoiesis.Molecular and cellular biology · 2022Article
- Localized glucose import, glycolytic processing, and mitochondria generate a focused ATP burst to power basement-membrane invasion.Developmental cell · 2022Article
- Regulation of Heme Synthesis by Mitochondrial Homeostasis Proteins.Frontiers in cell and developmental biology · 2022Review
- BCKDK Promotes Ovarian Cancer Proliferation and Migration by Activating the MEK/ERK Signaling Pathway.Journal of oncology · 2022Article
- Circular RNA circ-ERBB2 Elevates the Warburg Effect and Facilitates Triple-Negative Breast Cancer Growth by the MicroRNA 136-5p/Pyruvate Dehydrogenase Kinase 4 Axis.Molecular and cellular biology · 2021Article
- Fueling Cell Invasion through Extracellular Matrix.Trends in cell biology · 2021Review
- The mitochondrial landscape of ovarian cancer: emerging insights.Carcinogenesis · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
14 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent advances in tumor metabolism have revealed that metabolic reprogramming could dramatically promote caner metastasis. However, the relation and mechanism between metastasis and metabolic reprogramming are not thoroughly explored. Cell proliferation, colony formation, and invasion analysis were performed to evaluate the role of FAM210B in human cancer cells. Human ovarian cancer xenograft model was used to determine the effects of inhibiting FAM210B by shRNA on tumor metastasis. Microarray analysis was used to determine the target genes of FAM210B. FAM210B cellular localization was performed by mitochondria isolation and mitochondria protein extraction. To detect FAM210B-mediated metabolic reprogramming, oxygen consumption rate and extracellular acidification rate were measured. Our previous study screened a novel cancer progression-suppressor gene, FAM210B, which encodes an outer mitochondrial membrane protein, by the suppression of mortality by antisense rescue technique (SMART). Here we demonstrated that FAM210B loss was significantly associated with cancer metastasis and decreased survival in a clinical setting. Additionally, it was found that low expression of FAM210B was significantly correlated with decreased survival and enhanced metastasis in vivo and in vitro, and the loss of FAM210B led to an increased mitochondrial respiratory capacity and reduced glycolysis through the downregulation of pyruvate dehydrogenase kinase 4 (PDK4), which activated the EMT program and enhanced migratory and invasive properties. Collectively, our data unveil a potential metabolic target and mechanism of cancer metastasis.
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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.