Gingerol sensitizes TRAIL-induced apoptotic cell death of glioblastoma cells

Lee, Dae-Hee; Kim, Dong-Wook; Jung, Chang-Hwa; Lee, Yong J.; Park, Daeho

doi:10.1016/j.taap.2014.06.030

Cited by 60 publications

(33 citation statements)

References 42 publications

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“…Furthermore, sodium butyrate (a Histone deacetylase inhibitor) [42], as well as Rottlerin [43], were demonstrated to reduce the levels of XIAP and survivin through CDC2 suppression. Very recently, gingerol was also shown to induce TRAIL-associated apoptosis, by up-regulating TRAIL receptors (DR4, DR5) on one hand and down-regulating Bcl-2 and survivin on the other hand [44]. The concept of increasing TRAIL receptors is further enhanced by the synergistic use of TRAIL and the well known drugs salinomycin [45] and paclitaxel [46] which appeared to stimulate DR4, DR5 expression, thus increasing responsiveness of gliomas to TRAIL.…”

Section: Tumor Necrosis Factor (Tnf)mentioning

confidence: 99%

Pathophysiological mechanisms regulated by cytokines in gliomas

2015

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Section: Tumor Necrosis Factor (Tnf)mentioning

confidence: 99%

Pathophysiological mechanisms regulated by cytokines in gliomas

2015

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“…Many plant-derived compounds as cucurmin 5 , gingerol 6 and silibinin 7 , have been reported to restrain tumor growth in a series of experiments. Ellagic acid (EA) is a natural phenol present in many fruits and vegetables as cranberries, strawberries, blackberries, raspberries, grapes, and walnuts et al 8.…”

Section: Introductionmentioning

confidence: 99%

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

et al. 2016

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PURPOSE:To investigate the anticancer activity of ellagic acid (EA) in U251 human glioblastoma cells and its possible molecular mechanism. METHODS:The cells were treated with EA at various concentrations for different time periods. Cell viability and cell proliferation were detected by cell counting kit-8(CCK-8) assay and live/dead assay respectively. Cell apoptosis were measured with Annexin V-FITC/PI double staining method by flow cytometry and Mitochondrial membrane potential assay separately. Cell cycle was measured with PI staining method by flow cytometry. The expressions of Bcl-2, Survivin, XIAP, Caspase-3, Bax, JNK, p-JNK, ERK1/2, p-ERK1/2, p38, p-p38, DR4, DR5, CHOP and GRP78-related proteins were detected by western blot after EA treatment. RESULTS:Cell viability and proliferation of glioblastoma cells treated with EA were significantly lower than the control group. EA caused robust apoptosis of the glioblastoma cells compared to the control group. EA significantly decreased the proportion at G0/ G1 phases of cell cycling accompanied by increased populations at S phase in U251 cell lines. And the expressions of anti-apoptotic proteins were dramatically down-regulated. CONCLUSION:Ellagic acid potentially up-regulated DR4, DR5 and MAP kinases (JNK, ERK1/2 and p38). EA also caused significant increase in the expressions of CHOP and GRP78. Our findings suggest that EA would be beneficial for the treatment of glioblastoma.

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“…Natural compounds such as kurarinone (20), icaritin (21), withanolide E (22) were reported to downregulate cFLIP expression and subsequent sensitization of TRAIL-resistant cancer cells to TRAIL-induced apoptosis. Natural compounds, such as silibinin (23), gingerol (24) and indomethacin (25) were reported to possess both mechanisms of sensitizing TRAIL-resistant cancer cells.…”

Section: Introductionmentioning

confidence: 99%

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

Sophonnithiprasert

Nilwarangkoon

Nakamura

et al. 2015

International Journal of Oncology

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Abstract. The combination of TNF-related apoptosis-inducing ligand (TRAIL) and bioactive compound to enhance apoptosis in TRAIL-resistant cancer is one of cancer treatment strategies. TRAIL possesses the unique capacity to selectively induce apoptosis in cancer cells both in vitro and in vivo with little effect on normal cells. Recent studies have reported that there are many TRAIL-resistant cancers. Thus, bioactive compounds that enhance cytotoxicity of TRAIL would be potential candidates for cancer therapeutic application. This study evaluated the cytotoxic and apoptosis induction upon combined treatment of TRAIL and goniothalamin, the natural styryl-lactone compound extracted from plant Goniothalamus spp., in LoVo cells. The results showed that a combination of goniothalamin and TRAIL enhanced caspase-dependent apoptosis induction in LoVo cells via both death receptor-and mitochondrial-mediated apoptosis pathways. In addition, goniothalamin enhanced TRAIL-induced apoptosis through increased death receptor DR5 expression and decreased anti-apoptotic regulator cFLIP. Interestingly, goniothalamin increased translocation of DR5 to cell surface and consequently contributed to the enhancement of TRAIL-induced apoptosis. In conclusion, this is the first report showing the combined treatment of goniothalamin and TRAIL was able to effectively enhance TRAIL-mediated apoptosis induction in TRAIL-refractory colorectal cancer, LoVo cells. Therefore, this study may offer a strategic cancer treatment against TRAIL-resistant cancers.

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Gingerol sensitizes TRAIL-induced apoptotic cell death of glioblastoma cells

Cited by 60 publications

References 42 publications

Pathophysiological mechanisms regulated by cytokines in gliomas

Pathophysiological mechanisms regulated by cytokines in gliomas

Ellagic acid inhibits proliferation and induces apoptosis in human glioblastoma cells

Goniothalamin enhances TRAIL-induced apoptosis in colorectal cancer cells through DR5 upregulation and cFLIP downregulation

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