ArticleBiochemical and biophysical research communications2007
Induction of apoptosis by tumor suppressor FHIT via death receptor signaling pathway in human lung cancer cells.
Article in Biochemical and biophysical research communications, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 25 citations in OpenAlex.
- N-Terminal Domain of Fragile Histidine Triad Exerts Potent Cytotoxic Effect in HT1080 Cells and Increases Doxorubicin Cytotoxicity.Iranian journal of pharmaceutical research : IJPR · 2019Article
- Association of FHIT expression andOncoTargets and therapy · 2017Article
- Genetic and Chromosomal Aberrations and Their Clinical Significance in Renal Neoplasms.BioMed research international · 2015Review
- Computational Survey of FHIT, A Putative Human Tumor Suppressor, Truncates Structure.Avicenna journal of medical biotechnology · 2014Article
- The roles of sphingosine kinase 1 and 2 in regulating the metabolome and survival of prostate cancer cells.Biomolecules · 2013Article
- The roles of sphingosine kinases 1 and 2 in regulating the Warburg effect in prostate cancer cells.Cellular signalling · 2013Article
- Mitochondrial Ca(2+) and apoptosis.Cell calcium · 2012Review
- The effect of adenovirus-mediated gene expression of FHIT in small cell lung cancer cells.Cancer investigation · 2011Article
- Adenoviral vector-based strategies for cancer therapy.Current drug therapy · 2009Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
FHIT is a novel tumor suppressor gene located at human chromosome 3p14.2. Restoration of wild-type FHIT in 3p14.2-deficient human lung cancer cells inhibits cell growth and induces apoptosis. In this study, we analyzed potential upstream/downstream molecular targets of the FHIT protein and found that FHIT specifically targeted and regulated death receptor (DR) genes in human non-small-cell lung cancer (NSCLC) cells. Exogenous expression of FHIT by a recombinant adenoviral vector (Ad)-mediated gene transfer upregulated expression of DR genes. Treatment with a recombinant TRAIL protein, a DR-specific ligand, in Ad-FHIT-transduced NSCLC cells considerably enhanced FHIT-induced apoptosis, further demonstrating the involvement of DRs in FHIT-induced apoptosis. Moreover, we also found that FHIT targeted downstream of the DR-mediated signaling pathway. FHIT overexpression disrupted mitochondrial membrane integrity and activated multiple pro-apoptotic proteins in NSCLC cell. These results suggest that FHIT induces apoptosis through a sequential activation of DR-mediated pro-apoptotic signaling pathways in human NSCLC cells.
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Registered trials
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.