TRAIL-induced cell death and caspase-8 activation are inhibited by cisplatin but not carboplatin

Han, Soo Jeong; Ahn, Tae Kyu; Choi, Han Song; Shin, Jin Na; Piya, Sujan; Kim, Tae Hyoung

doi:10.3802/jgo.2009.20.2.113

Cited by 6 publications

(3 citation statements)

References 12 publications

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“…Contradictory studies demonstrating a cisplatin-mediated inhibition of TRAIL-induced cell death through direct inactivation of caspases have also been reported. The authors explain the discrepancy in their results compared to the majority of literature by the dependance on the duration of the treatment [49,50]. In our study, cisplatin was responsible for significant potentiation of TRAIL-induced apoptosis in human prostate and colon cancer cell lines.…”

Section: La-12 or Cisplatin-mediated Increase Of Dr5 Is Essential For Potentiation Of Trail-induced Caspase-8 Activation And Apoptosis Incontrasting

confidence: 54%

Cisplatin and a potent platinum(IV) complex-mediated enhancement of TRAIL-induced cancer cells killing is associated with modulation of upstream events in the extrinsic apoptotic pathway

Blanářová¹,

Jelínková²,

Szöór

et al. 2010

Carcinogenesis

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TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) can selectively trigger apoptosis in various cancer cell types. However, many cancer cells are resistant to death receptor-mediated apoptosis. Combination therapy with platinum complexes may affect TRAIL-induced signaling via modulation of various steps in apoptotic pathways. Here, we show that cisplatin or a more potent platinum(IV) complex LA-12 used in 20-fold lower concentration enhanced killing effects of TRAIL in human colon and prostate cancer cell lines via stimulation of caspase activity and overall apoptosis. Both platinum complexes increased DR5 surface expression in colon cancer cells. Small interfering RNA-mediated DR5 silencing rescued cells from sensitizing effects of platinum drugs on TRAIL-induced caspase-8 activation and apoptosis, showing the functional importance of DR5 in the effects observed. In addition, both cisplatin and LA-12 triggered the relocalization of DR4 and DR5 receptors to lipid rafts and accelerated internalization of TRAIL, which may also affect TRAIL signaling. Collectively, modulations of the initial steps of the extrinsic apoptotic pathway at the level of DR5 and plasma membrane are important for sensitization of colon and prostate cancer cells to TRAIL-induced apoptosis mediated by LA-12 and cisplatin.

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Section: La-12 or Cisplatin-mediated Increase Of Dr5 Is Essential For Potentiation Of Trail-induced Caspase-8 Activation And Apoptosis Incontrasting

confidence: 54%

Cisplatin and a potent platinum(IV) complex-mediated enhancement of TRAIL-induced cancer cells killing is associated with modulation of upstream events in the extrinsic apoptotic pathway

Blanářová¹,

Jelínková²,

Szöór

et al. 2010

Carcinogenesis

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“…Caspase-9 activity was detected after 3 h followed that by caspase-3 activity at 12 h, implying activation of caspase-9 prior to caspase-3. This activity profile was found similar to carboplatin response [ 21 , 22 ]. The aforementioned findings indicate that both the lectins, Bh L and Di L9 induced caspase-dependent apoptosis in a similar manner where caspase-9 is strongly activated.…”

Section: Resultsmentioning

confidence: 52%

Two Chitotriose-Specific Lectins Show Anti-Angiogenesis, Induces Caspase-9-Mediated Apoptosis and Early Arrest of Pancreatic Tumor Cell Cycle

et al. 2016

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The antiproliferative activity of two chito- specific agglutinins purified from Benincasa hispida (BhL) and Datura innoxia (DiL9) of different plant family origin was investigated on various cancer cell lines. Both lectins showed chitotriose specificity, by inhibiting lectin hemagglutinating activity. On further studies, it was revealed that these agglutinins caused remarkable concentration-dependent antiproliferative effect on human pancreatic cancerous cells but not on the normal human umbilical vein endothelial cells even at higher doses determined using MTT assay. The GI50 values were approximately 8.4 μg ml-1 (0.247 μM) and 142 μg ml-1(14.8 μM) for BhL and DiL9, respectively, against PANC-1 cells. The growth inhibitory effect of these lectins on pancreatic cancer cells were shown to be a consequence of lectin cell surface binding and triggering G0/G1 arrest, mitochondrial membrane depolarization, sustained increase of the intracellular calcium release and the apoptotic signal is amplified by activation of caspases executing cell death. Interestingly, these lectins also showed anti-angiogenic activity by disrupting the endothelial tubulogenesis. Therefore, we report for the first time two chito-specific lectins specifically binding to tumor glycans; they can be considered to be a class of molecules with antitumor activity against pancreatic cancer cells mediated through caspase dependent mitochondrial apoptotic pathway.

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“…It has been observed that soluble TRAIL mostly causes apoptosis in tumor cells but not in normal tissues (19). In previous reports, the application of a combined medication for tumor cells with TRAIL and drugs has been evaluated for whether TRAIL could synergize with chemotherapeutic drugs (20)(21)(22).…”

Section: Introductionmentioning

confidence: 99%

The Antitumor Effect of Gene-Engineered Exosomes in the Treatment of Brain Metastasis of Breast Cancer

Liu

Chen

2020

Front. Oncol.

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Strategies for treating brain metastases of breast cancer have demonstrated limited efficacy due to the blood-brain barrier (BBB). Gene therapy could improve the efficacy of chemotherapeutic drugs. Exosomes derived from the mesenchymal stem cells (MSCs) are small membrane-based gene vectors that can pass through the BBB. CXCR4 is the most commonly found chemokine receptor in human cancer cells. Furthermore, the SDF-1/CXCR4 axis plays an important role in the homing of MSCs for tumor cell diffusion and metastasis. TRAIL can selectively induce apoptosis in transformed cells without significant toxic side effects in normal tissues. In this study, exosomes were isolated from MSC CXCR4+TRAIL transduced with CXCR4 and TRAIL using a lentiviral vector. Synergistic antitumor study showed that exosome CXCR4+TRAIL exerted significant activity as a cooperative agent with carboplatin in an MDA-MB-231Br SCID mouse model, potentially engendering a novel strategy for advancing the treatment of brain metastases of breast cancer. Based on this study, further investigation of the effect of the vector on BBB and inducing apoptosis of brain tumors is warranted. In addition, the safety of the vector in animals during the treatment needs to be evaluated.

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TRAIL-induced cell death and caspase-8 activation are inhibited by cisplatin but not carboplatin

Cited by 6 publications

References 12 publications

Cisplatin and a potent platinum(IV) complex-mediated enhancement of TRAIL-induced cancer cells killing is associated with modulation of upstream events in the extrinsic apoptotic pathway

Cisplatin and a potent platinum(IV) complex-mediated enhancement of TRAIL-induced cancer cells killing is associated with modulation of upstream events in the extrinsic apoptotic pathway

Two Chitotriose-Specific Lectins Show Anti-Angiogenesis, Induces Caspase-9-Mediated Apoptosis and Early Arrest of Pancreatic Tumor Cell Cycle

The Antitumor Effect of Gene-Engineered Exosomes in the Treatment of Brain Metastasis of Breast Cancer

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