Apoptosis-resistant Mitochondria in T Cells Selected for Resistance to Fas Signaling

Wang, Gui Qiang; Gastman, Brian; Wieckowski, Eva; Goldstein, Leslie A.; Rabinovitz, Asaf; Yin, Xiao Ming; Rabinowich, Hannah

doi:10.1074/jbc.m006222200

Cited by 34 publications

(30 citation statements)

References 56 publications

(19 reference statements)

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“…For example, cells selected for resistance to Fas were completely cross-resistant to VP-16 or staurosporin (20). However, our TRAIL-resistant clones were not cross-resistant to either Fas or chemotherapeutic drugs such as paclitaxel.…”

Section: Discussionmentioning

confidence: 96%

“…All of them showed similar resistance to TRAIL as their parental clone R4 (data not shown). It has been reported that in vitro selection for resistance to some apoptosisinducing stimuli may result in cross-resistance to other cytotoxic agents (20,22). To determine whether our resistant clones also co-selected for resistance to Fas and paclitaxel, the parental SW480 cells and the resistant clones R4, R6, and R10 were treated with TRAIL, Fas, or paclitaxel.…”

Section: Trail-resistant Sw480 Colon Cancer Cells Selected After Prolmentioning

confidence: 99%

“…Mutation of the Bcl-2 family member Bax can confer resistance to TRAIL induced apoptosis in HCT116 cells (19). It also has been reported that Jurkat cells acquire resistance to Fas-mediated apoptosis because their mitochondria lose the ability to release intermembrane proteins in response to Bid or Bax (20). Both HCT116 and Jurkat cells behave as Type II cells in which the mitochondrial pathway appears to play a major role in death receptor-mediated apoptosis.…”

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confidence: 99%

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Deficient Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) Death Receptor Transport to the Cell Surface in Human Colon Cancer Cells Selected for Resistance to TRAIL-induced Apoptosis

Jin

McDonald

Dicker

et al. 2004

Journal of Biological Chemistry

210

150

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Many tumor cell types are sensitive to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis. Incubation of TRAIL-sensitive cells with TRAIL invariably leads to resistant survivors even when high doses of TRAIL are used. Because the emergence of resistance to apoptosis is a major concern in successful treatment of cancer, and TRAIL survivors may contribute to therapeutic failure, we investigated potential resistance mechanisms. We selected TRAILresistant SW480 human colon adenocarcinoma cells by repeatedly treating them with high and/or low doses of TRAIL. The resulting TRAIL-resistant clones were not cross-resistant to Fas or paclitaxel. Expression of modulators of apoptosis was not changed in the resistant cells, including TRAIL receptors, cFLIP, Bax, Bid, or IAP proteins. Surprisingly, we found that DISC formation was deficient in multiple selected TRAIL-resistant clones. DR4 was not recruited to the DISC upon TRAIL treatment, and caspase-8 was not activated at the DISC. Although total cellular DR4 mRNA and protein were virtually identical in TRAIL-sensitive parental and TRAIL-resistant clones, DR4 protein expression on the cell surface was essentially undetectable in the TRAILresistant clones. Moreover, exogenous DR4 and KILLER/DR5 were not properly transported to the cell surface in the TRAIL-resistant cells. Interestingly, TRAIL-resistant cells were resensitized to TRAIL by tunicamycin pretreatment, which increased cell surface expression of DR4 and KILLER/DR5. Our data suggest that tumor cells may become resistant to TRAIL through regulation of the death receptor cell surface transport and that resistance to TRAIL may be overcome by the glycosylation inhibitor/endoplasmic reticulum stressinducing agent tunicamycin.

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Section: Discussionmentioning

confidence: 96%

Section: Trail-resistant Sw480 Colon Cancer Cells Selected After Prolmentioning

confidence: 99%

mentioning

confidence: 99%

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Deficient Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) Death Receptor Transport to the Cell Surface in Human Colon Cancer Cells Selected for Resistance to TRAIL-induced Apoptosis

Jin

McDonald

Dicker

et al. 2004

Journal of Biological Chemistry

210

150

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“…Our data also showed that Naph induced apoptosis by increasing DNA fragmentation, nuclear condensation, and cell morphological changes by DAPI staining. In the process of apoptosis, caspases have been reported to be activated via both the extrinsic and intrinsic cell death pathways (20,21). In particular, the activation of caspase-3 is commonly involved in the apoptosis process in various cell types.…”

Section: Discussionmentioning

confidence: 99%

Novel anti-cancer role of naphthazarin in human gastric cancer cells

Son

2011

Int J Oncol

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Abstract. Gastric cancer is one of the most common malignant tumors and the second cause of cancer-related deaths worldwide. Naphthoquinones such as juglone and plumbagin are compounds used extensively to overcome resistance to chemotherapeutic agents in cancers due to their cytotoxic role. This study is the first to investigate the anti-cancer effect of naphthazarin (Naph), one of the naphthaquinones, in human gastric cancer AGS cells. We showed that Naph exhibited effective preferential cell growth inhibition via G2/M phase arrest and apoptosis, which was associated with reduced levels of Cdc2 and Cdc25C expression. Naph also increased cleaved caspase-3 and Poly ADR(adenosine diphosphate ribose) Polymerase expression, γ-H2AX expression (an indicator of DNA double strand breaks) and DNA fragmentation. We also found the generation of reactive oxygen species is a critical mediator in Naph-induced cell growth inhibition and apoptosis. The non-protein antioxidant, glutathione significantly abolished Naph-mediated inhibition of cell growth and apoptosis. Taken together, our findings showed that Naph not only inhibited cell growth, but also induced apoptosis of AGS cells, suggesting that Naph may be a potential candidate for cancer therapy against gastric cancers.

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“…It also contributes to resistance of GBM to therapy and leads to escape of tumor cells from surveillance by the immune system [115]. During apoptosis, caspases are activated to cleavage cellular substrates and lead to biochemical and morphological changes that are characteristics of apoptosis [116,117]. There are two major pathways by which caspase activation occurs: via the extrinsic pathways and the intrinsic pathway.…”

Section: Apoptosis and Bim In Glioblastomamentioning

confidence: 99%

Identification and Characterization of miR-148a as a New Oncogenic and Prognostic microRNA in Glioblastoma

Kim

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Great interest persists in useful prognostic and therapeutic targets in glioblastoma (GBM), the most common and most deadly human brain tumor. In this study, we report the identification and characterization of microRNA-148a (miR-148a) as a novel prognostic oncomiR in GBM. We show that miR-148a expression is elevated in human GBM specimens, cell lines, and stem cells (GSC) compared with normal human brain and astrocytes. High levels of miR-148a were a risk indicator for GBM patient survival. Functionally, miR-148a expression increased cell growth, survival, migration, and invasion in glioblastoma cells and GSCs and promoted GSC neurosphere formation. We identified two direct targets of miR-148a, the EGF receptor (EGFR) regulator MIG6 and the apoptosis regulator BIM. Rescue experiments showed that MIG6 and BIM were essential to mediate the oncogenic activity of miR-148a. By inhibiting MIG6 expression, miR148a reduced EGFR trafficking to Rab7-expressing compartments, which includes late endosomes and lysosomes. This process coincided with reduced degradation and elevated expression and activation of EGFR. Finally, inhibition of miR-148a strongly suppressed GSC and glioblastoma xenograft growth in vivo. Taken together, our findings provide a comprehensive analysis of the prognostic value and oncogenic function of miR-148a in glioblastoma, further defining it as a potential target for glioblastoma therapy.

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Apoptosis-resistant Mitochondria in T Cells Selected for Resistance to Fas Signaling

Cited by 34 publications

References 56 publications

Deficient Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) Death Receptor Transport to the Cell Surface in Human Colon Cancer Cells Selected for Resistance to TRAIL-induced Apoptosis

Deficient Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) Death Receptor Transport to the Cell Surface in Human Colon Cancer Cells Selected for Resistance to TRAIL-induced Apoptosis

Novel anti-cancer role of naphthazarin in human gastric cancer cells

Identification and Characterization of miR-148a as a New Oncogenic and Prognostic microRNA in Glioblastoma

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