Ionizing Radiations Induce Apoptosis in TRAIL Resistant Cancer Cells: in vivo and in vitro Analysis

Silva, Marcela Fernandes; Khokhar, Abdur Rehman; Qureshi, Muhammad Zahid; Farooqı, Ammad Ahmad

doi:10.7314/apjcp.2014.15.5.1905

Cited by 12 publications

(9 citation statements)

References 19 publications

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“…These results suggested that PDGFR-β-targeted therapy combined with RT was able to reduce the expression of cyclin B1, thereby blocking cells in the G2/M period and increasing the radiosensitivity of the cells. Apoptosis is regulated by the programmed cell death gene and is the main form of tumor cell death induced by radiation therapy (24). The present study demonstrated that the apoptosis index of the KD+RT group was higher than the other three groups, and that this group had the most TUNEL-positive cells.…”

Section: A B C Dmentioning

confidence: 45%

Silencing platelet-derived growth factor receptor-β enhances the radiosensitivity of C6 glioma cells in vitro and in vivo

et al. 2017

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Abstract. Platelet-derived growth factor receptor (PDGFR)-β is an important tyrosine kinase and its downregulation has been reported to alter the radiosensitivity of glioma cells, although the underlying mechanism is unclear. In order to investigate the effect of PDGFR-β on the radiosensitivity of glioblastoma, the present study transfected C6 glioma cells with a PDGFR-β-specific small interfering (si)RNA expression plasmid, and downregulation of the expression of PDGFR-β in C6 glioma cells was confirmed by western blotting and immunohistochemical analysis. Clone formation assays and xenograft growth curves demonstrated that PDGFR-β-siRNA enhanced the radiosensitivity of C6 glioma cells in vitro and in vivo. Furthermore, MTT and xenograft growth curves demonstrated that PDGFR-β-siRNA inhibited the proliferation of C6 glioma cells in vitro and in vivo, and terminal deoxynucleotidyl transferase dUTP nick end-labeling and immunohistochemical analyses demonstrated that PDGFR-β-siRNA induced apoptosis and inhibited the expression of Ki-67, cyclin B1 and vascular endothelial growth factor in C6 glioma cell xenografts. Taken together, these results suggested that PDGFR-β may be used as a target for the radiosensitization of glioblastoma.

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Section: A B C Dmentioning

confidence: 45%

Silencing platelet-derived growth factor receptor-β enhances the radiosensitivity of C6 glioma cells in vitro and in vivo

et al. 2017

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“…Tolerance to radiation has become one of the most challenging problems in cancer therapy. Cells undergo a complicated pathophysiological process after receiving radiation, involving abnormal activation of multiple signaling pathways (Jung et al, 2010;Xu et al, 2011), DNA damage of genes, the abnormal expression of proteins with the capacity of promoting DNA repair (Kasid et al, 1987;Kitahara et al, 2002;Fukuda et al, 2004), angiogenesis (Magnon et al, 2007), autophagy (Chaachouay et al, 2011;Zhuang et al, 2011), and apoptosis (Silva et al, 2014). Although these findings help to raise awareness and understanding of the cell radiosensitivity, the mechanism of this process is not clear.…”

Section: Discussionmentioning

confidence: 99%

Study of the radiotherapy sensitization effects and mechanism of capecitabine (Xeloda) against non-small-cell lung cancer cell line A549

Zhu

J²,

Sun

et al. 2015

Genet. Mol. Res.

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ABSTRACT. The purpose of this study was to explore the radiotherapy sensitization effects and the mechanism of capecitabine (Xeloda) against the non-small-cell lung cancer cell line, A549. γ-[ 60 Co] radiation was used as the intervention method. Proliferative inhibition of capecitabine on A549 cells was determined by the CCK-8 method. The effects of capecitabine on the apoptosis rate and cell cycle distribution of A549 were detected with the flow cytometric method. We found that capecitabine inhibited the proliferation of A549 in a dose-dependent manner, notably increased the cell apoptosis rate and blocked the cellular G0/G1 phase after radiotherapy by γ-[ 60 Co]. Therefore, capecitabine can significantly increase the radiosensitivity of A549; its mechanism may be related to cell cycle arrest and induction of apoptosis.

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“…There is a list of newly emerging scientific evidence highlighting molecular mechanisms to enhance or restore TRAIL induce apoptosis in cancer cells (Zhao et al, 2011;Huang et al, 2012;Jiang et al, 2013;Silva et al, 2014). Wide ranging phytochemicals are currently being tested for efficacy.…”

Section: Crosstalk Between Trail Induced Signaling Machinery and Automentioning

confidence: 99%

Dealing Naturally with Stumbling Blocks on Highways and Byways of TRAIL Induced Signaling

Rana¹,

Attar²,

Qureshi³

et al. 2014

Asian Pacific Journal of Cancer Prevention

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In-depth analysis of how TRAIL signals through death receptors to induce apoptosis in cancer cells using high throughput technologies has added new layers of knowledge. However, the wealth of information has also highlighted the fact that TRAIL induced apoptosis may be impaired as evidenced by experimental findings obtained from TRAIL resistant cancer cell lines. Overwhelmingly, increasing understanding of TRAIL mediated apoptosis has helped in identifying synthetic and natural compounds which can restore TRAIL induced apoptosis via functionalization of either extrinsic or intrinsic pathways. Increasingly it is being realized that biologically active phytochemicals modulate TRAIL induced apoptosis, as evidenced by cell-based studies. In this review we have attempted to provide an overview of how different phytonutrients have shown efficacy in restoring apoptosis in TRAIL resistant cancer cells. We partition this review into how the TRAIL mediated signaling landscape has broadened over the years and how TRAIL induced signaling machinery crosstalks with autophagic protein networks. Subsequently, we provide a generalized view of considerable biological activity of coumarins against a wide range of cancer cell lines and how coumarins (psoralidin and esculetin) isolated from natural sources have improved TRAIL induced apoptosis in resistant cancer cells. We summarize recent updates on piperlongumine, phenethyl isothiocyanate and luteolin induced activation of TRAIL mediated apoptosis. The data obtained from pre-clinical studies will be helpful in translation of information from benchtop to the bedside.

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Ionizing Radiations Induce Apoptosis in TRAIL Resistant Cancer Cells: in vivo and in vitro Analysis

Cited by 12 publications

References 19 publications

Silencing platelet-derived growth factor receptor-β enhances the radiosensitivity of C6 glioma cells in vitro and in vivo

Silencing platelet-derived growth factor receptor-β enhances the radiosensitivity of C6 glioma cells in vitro and in vivo

Study of the radiotherapy sensitization effects and mechanism of capecitabine (Xeloda) against non-small-cell lung cancer cell line A549

Dealing Naturally with Stumbling Blocks on Highways and Byways of TRAIL Induced Signaling

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