2019
DOI: 10.1002/jcb.28188
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Abstract: Fragile histidine trail (FHIT) is a tumor suppressor in response to DNA damage which has been deleted in various tumors. However, the signaling mechanisms and interactions of FHIT with regard to apoptotic proteins including p53 and p38 in the DNA damage-induced apoptosis are not well described. In the present study, we used etoposide-induced DNA damage in MCF-7 as a model to address these crosstalks. The time course study showed that the expression of FHIT, p53, and p38MAPK started after 1 hour following etopo… Show more

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Cited by 8 publications
(2 citation statements)
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“…It has been reported that etoposide induces cell death through an up-regulation of apoptosis ( 16 ). Thus, we investigated whether PEMFs enhance etoposide-induced cell death via an up-regulating apoptotic pathway.…”
Section: Resultsmentioning
confidence: 99%
“…It has been reported that etoposide induces cell death through an up-regulation of apoptosis ( 16 ). Thus, we investigated whether PEMFs enhance etoposide-induced cell death via an up-regulating apoptotic pathway.…”
Section: Resultsmentioning
confidence: 99%
“…Interestingly, etoposide has been previously observed to activate CD82 in a dosedependent manner via p53 and c-Jun, in human prostate cancer cell lines [94]. Moreover, etoposide has been shown in breast cancer cell lines to induce p53 expression which could then upregulate CD82 expression [95,96]. Thus, it may be meaningful to verify if etoposide upregulates CD82 expression in breast cancer patients, for repurposing as a therapeutic agent in treating a subset of non-metastatic breast cancer patients with low CD82 expression.…”
Section: Drugs Known To Target Cd82 Tyrosine Kinase Inhibitors (Tkis)mentioning
confidence: 98%