Title : Helicobacter pylori CagA protein activates Akt and attenuates chemotherapeutics-induced apoptosis in gastric cancer cells.

Pub. Date : 2017 Dec 26

PMID : 29371922






7 Functional Relationships(s)
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1 We investigate the effect of CagA on etoposide-induced apoptosis in gastric cancer cells to elucidate whether CagA play a role in gastric carcinogenesis via impairing DNA damage-dependent apoptosis. Etoposide S100 calcium binding protein A8 Homo sapiens
2 In the presence of etoposide, viability of parental AGS cells was decreased in a time-and dose-dependent manner, whereas CagA-expressing AGS cells were less susceptible to etoposide induced cell-killing effect. Etoposide S100 calcium binding protein A8 Homo sapiens
3 In the presence of etoposide, viability of parental AGS cells was decreased in a time-and dose-dependent manner, whereas CagA-expressing AGS cells were less susceptible to etoposide induced cell-killing effect. Etoposide S100 calcium binding protein A8 Homo sapiens
4 Suppression of etoposide-induced apoptosis was shown in CagA-expressing but not in parental AGS cells by DNA fragmentation, cell cycle, and annexin-V assays. Etoposide S100 calcium binding protein A8 Homo sapiens
5 This inhibitory effect of etoposide-induced apoptosis conferred by CagA was also demonstrated in SCM1 and MKN45 gastric cancer cell lines, with two additional chemotherapeutics, 5-FU and cisplatin. Etoposide S100 calcium binding protein A8 Homo sapiens
6 The effect of Akt activation on inhibition of etoposide-induced cytotoxicity by CagA was also evaluated. Etoposide S100 calcium binding protein A8 Homo sapiens
7 Enhancement of etoposide cytotoxicity by a PI-3-kinase inhibitor, LY294002, was evident in parental but was attenuated in CagA-expressing AGS cells. Etoposide S100 calcium binding protein A8 Homo sapiens