Resistance of mitochondrial DNA-deficient cells to TRAIL: role of Bax in TRAIL-induced apoptosis

Kim, Jayoung; Kim, Yun-Hee; Chang, Inik; Kim, Sunshin; Pak, Youngmi Kim; Oh, Byung‐Ha; Yagita, Hideo; Jung, Yong Keun; Oh, Young J.; Lee, Myung-Shik

doi:10.1038/sj.onc.1205406

Cited by 67 publications

(68 citation statements)

References 55 publications

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“…However, most 0 cells have been reported to undergo apoptosis as efficiently as their parental cells (4 -6). In contrast, we have reported that mtDNA-depleted hepatoma cells (SK-Hep1 0 cells) are resistant to TRAIL-induced apoptosis, which is consistent with the importance of mitochondria in cell death (7). However, it is not clearly elucidated how those cells with mitochondrial dysfunction resist cell death.…”

contrasting

confidence: 43%

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Park

Chang

Kim

et al. 2004

Journal of Biological Chemistry

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168

134

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contrasting

confidence: 43%

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Park

Chang

Kim

et al. 2004

Journal of Biological Chemistry

Self Cite

168

134

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“…Cell lines were examined for expression of proapoptotic Bax protein, which has been reported to be required for TRAIL-mediated apoptosis in some cell lines. 52,53 All cell lines we tested expressed substantial amounts of Bax (Fig 6), and again no correlation was found between relative Bax levels and TRAIL sensitivity.…”

Section: Death Ligand Gene Therapy Of Brain Tumor Cells S Rubinchik Ementioning

confidence: 86%

Enhanced apoptosis of glioma cell lines is achieved by co-delivering FasL-GFP and TRAIL with a complex Ad5 vector

Rubinchik

Woraratanadharm

et al. 2003

Cancer Gene Ther

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Brain tumors (BTs) are among the most malignant forms of human cancer. Unfortunately, current treatments are often ineffective and produce severe side effects. Cytotoxic gene therapy is an alternative treatment strategy, with the potential advantages of reduced toxicity to normal brain tissue. Apoptosis-inducing ''death ligands'' Fas ligand and TNF-related apoptosis-inducing ligand (TRAIL) are genes with substantial cytotoxic activity in susceptible tumor cells. Here, we compared the effectiveness of Ad vectormediated delivery of Fas ligand-green fluorescent protein (FasL-GFP) fusion protein, human TRAIL, and both genes simultaneously. We examined a panel of 13 cell lines (eight derived from primary isolates) for susceptibility to Ad5-based vector infection and for sensitivity to FasL-and TRAIL-mediated apoptosis. All cell lines were efficiently transduced, but, as expected, varied in their sensitivity to ligand-induced apoptosis. Generally, sensitivity to FasL-GFP correlated with cell surface FasR levels, but no such correlation was seen for TRAIL and its functional receptors, DR4 and DR5. The vector expressing both FasL-GFP and TRAIL was more effective than either of the single-gene vectors at comparable transduction levels, and it was effective against a broader range of cell lines. In five cell lines, coexpression resulted in apoptosis levels greater than those predicted for strictly additive activity of the two death ligands. We believe that Ad vector-mediated delivery of multiple death ligands may be developed as a potential BT therapy, either alone or in conjunction with surgical resection of the primary tumor.

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“…15,16 Others have shown that Bid can block the inhibitory effect of Bcl-2 on Fas-mediated apoptosis of HCC cells through oligomerizing Bak to release cytochrome c. 17 In SK-HEP-1 cells, TNF-related apoptosis-inducting ligand is known to induce the translocation of Bax, which subsequently leads to the cleavage of Bid. 18 Bid also has important functions in the development and chemotherapeutic sensitivity of HCC. Our previous experiments have shown that the level of Bid decreased in HCC tissues of patients except in poorly differentiated HCC in which cells may undergo a process of apoptosis or necrosis.…”

Section: Introductionmentioning

confidence: 99%

Therapeutic effect of α-fetoprotein promoter-mediated tBid and chemotherapeutic agents on orthotopic liver tumor in mice

Chen

Yip

et al. 2010

Gene Ther

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Previous studies have shown that the application of Ad/AFPtBid significantly and specifically killed hepatocellular carcinoma (HCC) cells in culture and subcutaneously implanted in mice. This study was to test the therapeutic efficacy of Ad/AFPtBid in an orthotopic hepatic tumor model. Four weeks after implantation of tumor cells into the liver, nude mice were treated with Ad/ AFPtBid alone or in combination with 5-fluorouracil (5-FU). Serum a-fetoprotein (AFP) was measured as a marker for tumor progression. The results showed that Ad/AFPtBid significantly inhibited Hep3B tumor growth. Ad/AFPtBid and 5-FU in combination was more effective than either agent alone. Tumor tissues of Ad/AFPtBid alone or combination treatment groups showed a decrease in cells positive for proliferation cell nuclear antigen, but an increase in apoptosis. Ad/AFPtBid did not suppress the hepatic tumor formed by non-AFP-producing hepatoma SK-HEP-1 cells or colorectal adenocarcinoma DLD-1 cells. The survival rate was higher in mice treated with Ad/AFPtBid plus 5-FU than those treated with either agent alone. No acute toxic effect was observed in mice receiving Ad/AFPtBid. Collectively, Ad/AFPtBid can specifically target and effectively suppress the AFP-producing orthotopic liver tumor in mice without obvious toxicity, indicating that it is a promising tool in combination with chemotherapeutic agents for treatment of AFP-producing HCC.

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Resistance of mitochondrial DNA-deficient cells to TRAIL: role of Bax in TRAIL-induced apoptosis

Cited by 67 publications

References 55 publications

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Resistance of Mitochondrial DNA-depleted Cells against Cell Death

Enhanced apoptosis of glioma cell lines is achieved by co-delivering FasL-GFP and TRAIL with a complex Ad5 vector

Therapeutic effect of α-fetoprotein promoter-mediated tBid and chemotherapeutic agents on orthotopic liver tumor in mice

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