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Cited by 4 publications
(6 citation statements)
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References 27 publications
(30 reference statements)
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“…Lung tumour cells are sensitive to treatments based on selective inhibitors of oxidative phosphorylation that act on the mitochondrial complex III, while these are ineffective when FHIT is present. erefore, an assessment of HSP60/HSP10 levels (in association with the expression of FHIT) appears fundamental in choosing the kind of therapy to be used against lung cancer [65][66][67][68][69] (Figure 1). target molecules are toll-like receptors, in particular TLR-4 and TLR-2.…”
Section: Fragile Histidine Triad (Fhit) Proteinmentioning
confidence: 99%
“…Lung tumour cells are sensitive to treatments based on selective inhibitors of oxidative phosphorylation that act on the mitochondrial complex III, while these are ineffective when FHIT is present. erefore, an assessment of HSP60/HSP10 levels (in association with the expression of FHIT) appears fundamental in choosing the kind of therapy to be used against lung cancer [65][66][67][68][69] (Figure 1). target molecules are toll-like receptors, in particular TLR-4 and TLR-2.…”
Section: Fragile Histidine Triad (Fhit) Proteinmentioning
confidence: 99%
“…Only more than a decade after its identification has our group identified a list of Fhit candidate partners, including among them, FRDX, HSP10 [ 4 ], and annexin A4 (A4) [ 5 ]. We also identified a short 7-aminoacids peptide from the Fhit protein that is still able to bind A4 and sensitize lung cancer cells to paclitaxel, thus recapitulating the activity of the full-length Fhit protein on A4 [ 6 , 7 ].…”
Section: Introductionmentioning
confidence: 99%
“…3,4 The restoration of FHIT in these cancerous cells suppresses tumorigenicity, induces cell-cycle arrest, increases the proapoptotic (Bax, Bad, and Bid), and lowers the level of Bcl-2 family (Bcl-2, Bcl-XL , and Mcl-1) [5][6][7] ; thus, FHIT gene therapy could be a new therapeutic approach for cancer treatment. 8 Many agents such as UV irradiation, alkylation of bases, chemotherapy, and oxidative stress are involved in DNA damage. 9 Etoposide, an inhibitor of topoisomerase II, is used in chemotherapy of cancer by inducing DNA damage and apoptosis.…”
Section: Introductionmentioning
confidence: 99%
“…Moreover, it has been shown the lack of FHIT expression or function in cancer cells has been correlated with the initiation and/or progression of tumors . The restoration of FHIT in these cancerous cells suppresses tumorigenicity, induces cell‐cycle arrest, increases the proapoptotic (Bax, Bad, and Bid), and lowers the level of Bcl‐2 family (Bcl‐2, Bcl‐ XL , and Mcl‐1); thus, FHIT gene therapy could be a new therapeutic approach for cancer treatment …”
Section: Introductionmentioning
confidence: 99%