2010
DOI: 10.1016/j.bcp.2010.01.032
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Bax deficiency mediated drug resistance can be reversed by endoplasmic reticulum stress induced death signaling

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Cited by 19 publications
(15 citation statements)
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“…The insulin resistant state was accompanied by hyperinsulinemia and abnormal glucose metabolism, both of which can induce ER stress by stimulating mitochondria to produce RoS. ER stress then inhibits insulin and reduces the expression of GLUTs, exacerbating IR [1,28,[31][32][33][34][35][36]. In this study, early IR was accompanied by increased production of intracellular RoS and decreased MMP, resulting in oxidative and ER stress.…”
Section: Discussionmentioning
confidence: 59%
See 1 more Smart Citation
“…The insulin resistant state was accompanied by hyperinsulinemia and abnormal glucose metabolism, both of which can induce ER stress by stimulating mitochondria to produce RoS. ER stress then inhibits insulin and reduces the expression of GLUTs, exacerbating IR [1,28,[31][32][33][34][35][36]. In this study, early IR was accompanied by increased production of intracellular RoS and decreased MMP, resulting in oxidative and ER stress.…”
Section: Discussionmentioning
confidence: 59%
“…Under normal conditions, hepatocellular carcinoma cells are not sensitive to chemoand radiotherapy, characterized by drug resistance and poor systemic effects of therapies. This may be due to the state of chronic stress caused by the liver tumor microenvironment, including underdeveloped vessels, anoxia, low glucose, and low pH [28,[32][33][34][35][36][39][40][41][42].…”
Section: Discussionmentioning
confidence: 99%
“…53 Indeed, certain chemical apoptotic stimuli recruit alternative forms of cell death in the absence of Bax and Bak 54, 55 and molecules able to induce cyt c release in the absence of Bax have also been identified. 23 This is not the case in our system, where in absence of Bax in colorectal cancer cells, PGC1α is not anymore able to induce cyt c release, apoptosis and to oppose tumor growth. We therefore believe that, in the presence of Bax, the PGC1α-induced ROS accumulation represents one of the main apoptosis-driving factors in colorectal cancer cells, thus bona fide opening the avenue for novel therapeutic strategies for the treatment of colon cancer.…”
Section: ©2 0 1 1 L a N D E S B I O S C I E N C E D O N O T D I S Tmentioning
confidence: 60%
“…17,[19][20][21] On the other hand, the absence of Bax alone is not sufficient to block apoptosis 19,21,22 and several candidates have been proposed that could alternatively induce cyt c release in the absence of Bax. 23 The relationship between ROS and Bax protein activation has been widely investigated. It has been postulated that Bax acts upstream of ROS production and that Bax-induced ROS burst is both necessary and sufficient for cyt c redistribution in these cells.…”
Section: Pgc1α Induces Bax Activationmentioning
confidence: 99%
“…26,27 Knowing that Grp78 has a role in ER stress, we investigated ER stress status in oridonin-treated HepG2 cells. Results showed that oridonin treatment activated ER stress.…”
Section: Discussionmentioning
confidence: 99%