c-Myc degradation induced by DNA damage results in apoptosis of CHO cells

Jiang, Mingyang; Li, Yuanchao; Yang, Ying; Wu, Jiarui

doi:10.1038/sj.onc.1206501

Cited by 23 publications

(26 citation statements)

References 36 publications

(33 reference statements)

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“…Tripchlorolide (TC), a derivate of triptolide with similar activity and much lower toxicity [25], has shown its anti-neoplastic activities against leukemic, lung and other tumor cells. Our previous works reported that TC disturbed the cell cycle and induced apoptosis in Chinese hamster ovary (CHO) cells, which resulted from degradation of c-Myc and dysfunctional p53 [26,27]. In this study, we demonstrated that TC inhibited the expression of viral oncoprotein E6/E7, which resulted in an up-regulation of p53 in HeLa S3 cells.…”

Section: Introductionmentioning

confidence: 59%

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

et al. 2005

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Recent studies indicate that cell-cycle checkpoints are tightly correlated with the regulation of apoptosis, in which p53 plays an important role. Our present works show that the expression of E6/E7 oncogenes of human papillomavirus in HeLa cells is inhibited in the presence of anti-tumor reagent tripchlorolide (TC), which results in the up-regulation of p53 in HeLa cells. Interestingly, under the same TC-treatment, the cells at the early S-phase are more susceptible to apoptosis than those at the middle S-phase although p53 protein is stabilized to the same level in both situations. Significant difference is exhibited between the two specified expression profiles. Further analysis demonstrates that anti-apoptotic gene survivin is up-regulated by p53 in the TC-treated middle-S cells, whereas it is down-regulated by p53 in the TC-treated early-S cells. Taken together, the present study indicates that the differential p53-regulated expression of survivin at different stages of the cell cycle results in different cellular outputs under the same apoptosis-inducer.

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Section: Introductionmentioning

confidence: 59%

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

et al. 2005

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“…Indeed, c-MYC overexpression from a transgene has been shown to inhibit the p53-dependent transcription of the cyclin-dependent kinase inhibitor p21 and thus potentially to regulate the outcome of the p53 response to DNA damage. 30 Some authors have reported a decrease in the level of c-MYC upon cell treatment with compounds targeting DNA, either by a degradation-dependent process 31 or a decline in c-MYC mRNA. 32 However, these observations were made at late time points contemporary of apoptosis and a careful analysis of the level of c-MYC at early time points of the DNA damage response was still lacking.…”

Section: Introductionmentioning

confidence: 99%

c-Myc protein is degraded in response to UV irradiation

Britton¹,

Salles²,

Calsou³

2008

Cell Cycle

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The c-MYC proto-oncogene encodes a transcription factor that is critical for cell growth and proliferation. It is one of the genes frequently altered in cancer cells in which it exhibits constitutive activity. The half-life of c-MYC is very short in quiescent cells due to ubiquitin-mediated proteolysis. We report here the rapid and dose-dependent decline of c-MYC protein level after UV-irradiation in various human and rodent cells. This decline is due to a proteasomal degradation of c-MYC protein and does not require the binding sites for the FBW7 and SKP2 ubiquitin ligases. Together, our data exclude a prominent role for the stress-responsive kinase PAK2, for the major phosphoinositide 3-kinase related protein kinases ATR, ATM, DNA-PK and mTOR and for ERK, JNK and p38 mitogen activated protein kinases in this UV-induced degradation process. We propose that c-MYC degradation is part of the global cell response to UV-damage, complementary to the accumulation and activation of the p53 transcription factor. By contributing to the replication arrest after infliction of lesions to the genome, the induced degradation of c-MYC may be part of the safeguard mechanisms maintaining genome stability.

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“…Comet assay showed that TC resulted in DNA damage of CHOC400 cells (data not shown). Moreover, UV41 cell line, which is deficient in the ERCC4 gene encoding a nucleotide repair protein, was much more sensitive to TC-treatment than the normal CHO cells (data not shown, see reference [22]). These results suggest that TC causes DNA damage and then triggers the apoptotic program of CHO cells.…”

Section: Discussionmentioning

confidence: 97%

Induction of mitochondrion-mediated apoptosis of CHO cells by tripchloro- lide

Ren

Xiong

2003

Cell Res

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Tripchlorolide (TC) is a potent antitumor reagent purified from a Chinese herb Tripterygium Wilfordii Hook. f.. However, its cellular effects and mechanism of action are unknown. We showed here that TC induced apoptosis of Chinese Hamster Ovary (CHO) cells in time-and dose-dependent manners. TC resulted in the degradation of Bcl-2, the translocation of Bax from the cytosol to mitochondria, and the release of cytochrome c from mitochondria. Stable overexpression of human Bcl-2 could reduce the apoptosis of TC-treated cells by blocking the translocation of Bax and the release of cytochrome c. These results indicate that TC induces apoptosis of CHO cell by activating the mitochondrion-mediated apoptotic pathway involving the proteins of Bcl-2 family and cytochrome c.

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c-Myc degradation induced by DNA damage results in apoptosis of CHO cells

Cited by 23 publications

References 36 publications

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

c-Myc protein is degraded in response to UV irradiation

Induction of mitochondrion-mediated apoptosis of CHO cells by tripchloro- lide

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