Fhit–Fdxr interaction in the mitochondria: modulation of reactive oxygen species generation and apoptosis in cancer cells

[1]  M. Protopopova,et al.  An inhibitor of oxidative phosphorylation exploits cancer vulnerability , 2018, Nature Medicine.

[2]  S. Volinia,et al.  The ubiquitous ‘cancer mutational signature’ 5 occurs specifically in cancers with deleted FHIT alleles , 2017, Oncotarget.

[3]  Santanu Banerjee,et al.  Proximal Ligation Assay (PLA) on Lung Tissue and Cultured Macrophages to Demonstrate Protein-protein Interaction. , 2017, Bio-protocol.

[4]  K. Huebner,et al.  Identification of Fhit as a post-transcriptional effector of Thymidine Kinase 1 expression. , 2017, Biochimica et biophysica acta. Gene regulatory mechanisms.

[5]  K. Huebner,et al.  Fragile Genes That Are Frequently Altered in Cancer: Players Not Passengers , 2017, Cytogenetic and Genome Research.

[6]  V. Papadopoulos,et al.  Adrenal Mitochondria and Steroidogenesis: From Individual Proteins to Functional Protein Assemblies , 2016, Front. Endocrinol..

[7]  F. Sotgia,et al.  Repurposing atovaquone: Targeting mitochondrial complex III and OXPHOS to eradicate cancer stem cells , 2016, Oncotarget.

[8]  K. Huebner,et al.  The FHIT gene product: tumor suppressor and genome “caretaker” , 2014, Cellular and Molecular Life Sciences.

[9]  C. Brenner,et al.  A knockdown with smoke model reveals FHIT as a repressor of Heme oxygenase 1 , 2014, Cell cycle.

[10]  D. Sabatini,et al.  Metabolic determinants of cancer cell sensitivity to glucose limitation and biguanides , 2014, Nature.

[11]  C. Croce,et al.  Fhit Delocalizes Annexin A4 from Plasma Membrane to Cytosol and Sensitizes Lung Cancer Cells to Paclitaxel , 2013, PloS one.

[12]  K. Huebner,et al.  Initiation of Genome Instability and Preneoplastic Processes through Loss of Fhit Expression , 2012, PLoS genetics.

[13]  C. Croce,et al.  Intramitochondrial calcium regulation by the FHIT gene product sensitizes to apoptosis , 2009, Proceedings of the National Academy of Sciences.

[14]  C. Croce,et al.  Fragile gene product, Fhit, in oxidative and replicative stress responses , 2009, Cancer science.

[15]  C. Croce,et al.  Fhit modulates the DNA damage checkpoint response. , 2006, Cancer research.

[16]  Y. Sugimoto,et al.  Gene expression of ferredoxin reductase predicts outcome in patients with metastatic colorectal cancer treated by 5-fluorouracil plus leucovorin , 2006, Cancer Chemotherapy and Pharmacology.

[17]  M. Macleod,et al.  Expression of common chromosomal fragile site genes, WWOX/FRA16D and FHIT/FRA3B is downregulated by exposure to environmental carcinogens, UV, and BPDE but not by IR , 2005, Molecular carcinogenesis.

[18]  D. Iliopoulos,et al.  Concordant loss of fragile gene expression early in breast cancer development , 2005, Pathology international.

[19]  T. Ørntoft,et al.  DNA damage response as a candidate anti-cancer barrier in early human tumorigenesis , 2005, Nature.

[20]  Dimitris Kletsas,et al.  Activation of the DNA damage checkpoint and genomic instability in human precancerous lesions , 2005, Nature.

[21]  S. Gupta,et al.  HSP60, Bax, Apoptosis and the Heart , 2005, Journal of cellular and molecular medicine.

[22]  C. Croce,et al.  Fhit-deficient normal and cancer cells are mitomycin C and UVC resistant , 2004, British Journal of Cancer.

[23]  J. Minna,et al.  Synergistic Tumor Suppression by Coexpression of FHIT and p53 Coincides with FHIT-Mediated MDM2 Inactivation and p53 Stabilization in Human Non-Small Cell Lung Cancer Cells , 2004, Cancer Research.

[24]  D. Iliopoulos,et al.  The fragile genes FHIT and WWOX are inactivated coordinately in invasive breast carcinoma , 2004, Cancer.

[25]  S. Korsmeyer,et al.  Review Cell Death: Critical Control Points Another Line of Evidence for the Importance of Caspases in Cell Death Came From , 2022 .

[26]  C. Croce,et al.  Fragile site orthologs FHIT/FRA3B and Fhit/Fra14A2: Evolutionarily conserved but highly recombinogenic , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[27]  G. Diaz,et al.  Mitochondrial localization of reactive oxygen species by dihydrofluorescein probes , 2003, Histochemistry and Cell Biology.

[28]  C. Croce,et al.  Regression of upper gastric cancer in mice by FHIT gene delivery , 2003, FASEB journal : official publication of the Federation of American Societies for Experimental Biology.

[29]  C. Croce,et al.  Designed FHIT alleles establish that Fhit-induced apoptosis in cancer cells is limited by substrate binding , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[30]  Xinbin Chen,et al.  The ferredoxin reductase gene is regulated by the p53 family and sensitizes cells to oxidative stress-induced apoptosis , 2002, Oncogene.

[31]  C. Croce,et al.  Restoration of fragile histidine triad (FHIT) expression induces apoptosis and suppresses tumorigenicity in lung and cervical cancer cell lines , 2002, Proceedings of the National Academy of Sciences of the United States of America.

[32]  K. Kinzler,et al.  Ferredoxin reductase affects p53-dependent, 5-fluorouracil–induced apoptosis in colorectal cancer cells , 2001, Nature Medicine.

[33]  C. Croce,et al.  The tumor spectrum in FHIT-deficient mice , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[34]  C. Croce,et al.  FHIT gene therapy prevents tumor development in Fhit-deficient mice , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[35]  C. Croce,et al.  Effect of adenoviral transduction of the fragile histidine triad gene into esophageal cancer cells. , 2001, Cancer research.

[36]  M. Paterson,et al.  Association of FHIT (fragile histidine triad), a candidate tumour suppressor gene, with the ubiquitin-conjugating enzyme hUBC9. , 2000, The Biochemical journal.

[37]  L. D. Barnes,et al.  The Tumor Suppressor Protein Fhit , 1999, The Journal of Biological Chemistry.

[38]  J. Minna,et al.  Induction of apoptosis and inhibition of tumorigenicity and tumor growth by adenovirus vector-mediated fragile histidine triad (FHIT) gene overexpression. , 1999, Cancer research.

[39]  C. Croce,et al.  Loss of FHIT function in lung cancer and preinvasive bronchial lesions. , 1998, Cancer research.

[40]  L. D. Barnes,et al.  Replacement of Fhit in cancer cells suppresses tumorigenicity. , 1997, Proceedings of the National Academy of Sciences of the United States of America.

[41]  J. Roth,et al.  Delivery of the p53 tumor suppressor gene into lung cancer cells by an adenovirus/DNA complex. , 1997, Cancer gene therapy.

[42]  J. Samet,et al.  Molecular damage in the bronchial epithelium of current and former smokers. , 1997, Journal of the National Cancer Institute.

[43]  J S Lee,et al.  Clonal genetic alterations in the lungs of current and former smokers. , 1997, Journal of the National Cancer Institute.

[44]  C. Croce,et al.  The FHIT Gene, Spanning the Chromosome 3p14.2 Fragile Site and Renal Carcinoma–Associated t(3;8) Breakpoint, Is Abnormal in Digestive Tract Cancers , 1996, Cell.

[45]  D. Sklan,et al.  Electron leakage from the mitochondrial NADPH-adrenodoxin reductase-adrenodoxin-P450scc (cholesterol side chain cleavage) system. , 1993, Archives of biochemistry and biophysics.

[46]  K. Suzuki,et al.  Components of the electron transport system in adrenal steroid hydroxylase. Isolation and properties of non-heme iron protein (adrenodoxin). , 1967, The Journal of biological chemistry.

[47]  C. Croce,et al.  Muir-Torre-like syndrome in Fhit-deficient mice. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[48]  F. Hartl,et al.  Molecular chaperone functions of heat-shock proteins. , 1993, Annual review of biochemistry.