Literature DB >> 19514467

[FHIT--tumor suppressor protein involved in induction of apoptosis and cell cycle regulation].

Róza Pecherzewska1, Barbara Nawrot.   

Abstract

The fragile histidine triad (Fhit) protein is a diadenosine triphosphate hydrolase belonging to the histidine triad family of nucleotide-binding proteins. Fhit is a tumor suppressor protein which plays an important role in pro-apoptotic signalling, cell cycle control and sensitivity to DNA damaging agents. The Ap3A--hydrolase activity of Fhit is not required for exertion of its tumor suppressor function. The FHIT gene is located in FRA3B region--the most common fragile site in the human genome. Loss of FHIT is observed in a variety of tumors and in premalignant states. Re-expression of FHIT in human cancer cells leads to inhibition of tumorogenecity and restoration of caspase-dependent apoptosis. Viral-mediated FHIT gene therapy induces apoptosis and suppresses tumors in preclinical models. Therefore, treatment with the FHIT gene may constitute a novel clinical approach for gene therapy of human cancers.

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Year:  2009        PMID: 19514467

Source DB:  PubMed          Journal:  Postepy Biochem        ISSN: 0032-5422


  4 in total

1.  Cyclin-dependent kinase inhibitor 3 (CDKN3) novel cell cycle computational network between human non-malignancy associated hepatitis/cirrhosis and hepatocellular carcinoma (HCC) transformation.

Authors:  L Wang; L Sun; J Huang; M Jiang
Journal:  Cell Prolif       Date:  2011-06       Impact factor: 6.831

Review 2.  Fragile histidine triad protein: structure, function, and its association with tumorogenesis.

Authors:  Md Imtaiyaz Hassan; Abdullah Naiyer; Faizan Ahmad
Journal:  J Cancer Res Clin Oncol       Date:  2009-12-24       Impact factor: 4.553

Review 3.  Genetic Markers in Lung Cancer Diagnosis: A Review.

Authors:  Katarzyna Wadowska; Iwona Bil-Lula; Łukasz Trembecki; Mariola Śliwińska-Mossoń
Journal:  Int J Mol Sci       Date:  2020-06-27       Impact factor: 5.923

4.  Genome-wide association study of maternal and inherited loci for conotruncal heart defects.

Authors:  A J Agopian; Laura E Mitchell; Joseph Glessner; Angela D Bhalla; Anshuman Sewda; Hakon Hakonarson; Elizabeth Goldmuntz
Journal:  PLoS One       Date:  2014-05-06       Impact factor: 3.240

  4 in total

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