Title : Bid-overexpression regulates proliferation and phosphorylation of Akt and MAPKs in response to etoposide-induced DNA damage in hepatocellular carcinoma cells.

Pub. Date : 2012

PMID : 23093908






11 Functional Relationships(s)
Download
Sentence
Compound Name
Protein Name
Organism
1 Bid-overexpression regulates proliferation and phosphorylation of Akt and MAPKs in response to etoposide-induced DNA damage in hepatocellular carcinoma cells. Etoposide BH3 interacting domain death agonist Homo sapiens
2 However, the effects of Bid on hepatocellular carcinoma (HCC) cell proliferation in response to etoposide-induced DNA damage have not been sufficiently investigated. Etoposide BH3 interacting domain death agonist Homo sapiens
3 METHODS: Using a stable Bid-overexpression HCC cell line, Bid/PLC/PRF/5, overexpression of Bid promoted loss of viability in response to etoposide-induced DNA damage. Etoposide BH3 interacting domain death agonist Homo sapiens
4 METHODS: Using a stable Bid-overexpression HCC cell line, Bid/PLC/PRF/5, overexpression of Bid promoted loss of viability in response to etoposide-induced DNA damage. Etoposide BH3 interacting domain death agonist Homo sapiens
5 METHODS: Using a stable Bid-overexpression HCC cell line, Bid/PLC/PRF/5, overexpression of Bid promoted loss of viability in response to etoposide-induced DNA damage. Etoposide BH3 interacting domain death agonist Homo sapiens
6 RESULTS: The survival rates of 100 muM etoposide on the cells with control vector and Bid/PLC/PRF/5 at 48 hours amounted to 71% +- 0.75% and 59% +- 0.60% with MTT assay, and similar results of 85% +- 0.08% and 63% +- 0.14% with BrdU-labeling assay respectively. Etoposide BH3 interacting domain death agonist Homo sapiens
7 Moreover, overexpression of Bid sensitized the cells to apoptosis at a high dose of etoposide (causing irreparable damage). Etoposide BH3 interacting domain death agonist Homo sapiens
8 Overexpression of Bid suppressed the activation of Akt with respect to etoposide-induced DNA damage. Etoposide BH3 interacting domain death agonist Homo sapiens
9 CONCLUSION: Taken together, these results suggest that overexpression of Bid suppressed the activation of Akt, p38, and c-Jun, and promoted the activation of ERK1/2 induced by etoposide, suggesting that the promotion of ERK1/2 activation may have a negative effect on Bid-mediated HCC DNA damage induced by etoposide. Etoposide BH3 interacting domain death agonist Homo sapiens
10 CONCLUSION: Taken together, these results suggest that overexpression of Bid suppressed the activation of Akt, p38, and c-Jun, and promoted the activation of ERK1/2 induced by etoposide, suggesting that the promotion of ERK1/2 activation may have a negative effect on Bid-mediated HCC DNA damage induced by etoposide. Etoposide BH3 interacting domain death agonist Homo sapiens
11 CONCLUSION: Taken together, these results suggest that overexpression of Bid suppressed the activation of Akt, p38, and c-Jun, and promoted the activation of ERK1/2 induced by etoposide, suggesting that the promotion of ERK1/2 activation may have a negative effect on Bid-mediated HCC DNA damage induced by etoposide. Etoposide BH3 interacting domain death agonist Homo sapiens