2017
DOI: 10.1038/s41418-017-0008-0
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BOK promotes chemical-induced hepatocarcinogenesis in mice

Abstract: BCL-2-related ovarian killer (BOK) is a conserved and widely expressed BCL-2 family member with sequence homology to pro-apoptotic BAX and BAK, but with poorly understood pathophysiological function. Since several members of the BCL-2 family are critically involved in the regulation of hepatocellular apoptosis and carcinogenesis we aimed to establish whether loss of BOK affects diethylnitrosamine (DEN)-induced hepatocarcinogenesis in mice. Short-term exposure to DEN lead to upregulation of BOK mRNA and protein… Show more

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Cited by 30 publications
(42 citation statements)
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“…More recently, in a chemical (DEN)-induced model of liver carcinogenesis, loss of BOK has been shown to protect against cancer. In this model, cancer can be promoted by death of hepatocytes, supporting compensatory proliferation with associated mutagenesis, in surrounding tissue that ultimately leads to live cancer [ 114 ]. Interestingly, deletion of BOK inhibited the ER-stress response and induction of pro-apoptotic BH3-only proteins BIM and PUMA, placing BOK's tumour promoting role upstream of MOMP [ 114 ].…”
Section: Favoured Interactionsmentioning
confidence: 99%
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“…More recently, in a chemical (DEN)-induced model of liver carcinogenesis, loss of BOK has been shown to protect against cancer. In this model, cancer can be promoted by death of hepatocytes, supporting compensatory proliferation with associated mutagenesis, in surrounding tissue that ultimately leads to live cancer [ 114 ]. Interestingly, deletion of BOK inhibited the ER-stress response and induction of pro-apoptotic BH3-only proteins BIM and PUMA, placing BOK's tumour promoting role upstream of MOMP [ 114 ].…”
Section: Favoured Interactionsmentioning
confidence: 99%
“…In this model, cancer can be promoted by death of hepatocytes, supporting compensatory proliferation with associated mutagenesis, in surrounding tissue that ultimately leads to live cancer [ 114 ]. Interestingly, deletion of BOK inhibited the ER-stress response and induction of pro-apoptotic BH3-only proteins BIM and PUMA, placing BOK's tumour promoting role upstream of MOMP [ 114 ]. Secondly, BOK was also shown to have an additional growth-promoting effect, though the mechanisms underlying this remain unclear it would also be expected to be pro-tumourigenic [ 114 ].…”
Section: Favoured Interactionsmentioning
confidence: 99%
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“…Several studies suggest that BOK exerts its anti-tumorigenic effects through non-apoptotic functions [82,83]. On the other hand, a pro-tumorigenic role for BOK is reported in hepatocellular carcinoma where deletion of BOK is infrequent [84].…”
Section: Mechanisms Of Apoptotic De-regulationmentioning
confidence: 99%
“…This process helps promote the development and progression of liver cancer. The process involved many mechanisms such as oxidative stress, endoplasmic reticulum stress and mitochondrial damage, which will activate and promote the synthesis and secretion of tumor-related transcription factors and cytokines, resulting in DNA damage and further promoting tumorigenesis [15][16][17][18] .…”
Section: Inflammation and Liver Cancermentioning
confidence: 99%