ER stress induced by ionising radiation in IEC-6 cells

Zhang, Bo; Wang, Yan; Pang, Xiaowu; Su, Yongping; Ai, Guoping; Wang, Tao

doi:10.3109/09553001003668014

Cited by 62 publications

(53 citation statements)

References 25 publications

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“…A previous study demonstrated that ionizing radiation (IR) could induce up-regulation of ER stress markers, including GRP78 at the protein and mRNA levels in IEC-6 cells [26]. As shown in Fig.…”

Section: Effects Of Different Gen Concentrations On Grp78 Herp and Hmentioning

confidence: 91%

Radioprotective effects of genistein on HL-7702 cells via the inhibition of apoptosis and DNA damage

Liu

Cong

et al. 2015

Cancer Letters

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Section: Effects Of Different Gen Concentrations On Grp78 Herp and Hmentioning

confidence: 91%

Radioprotective effects of genistein on HL-7702 cells via the inhibition of apoptosis and DNA damage

Liu

Cong

et al. 2015

Cancer Letters

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“…As previously indicated ER is another target of radiation, radiation initially induces ROS production, which would activate ER membrane sensors of ER stress in IEC-6 cells and breast cancer MDA-MB-231 and MCF-7 cells (76,77). ER stress induced by radiation triggers signal transduction pathways, known as unfolded protein response (UPR) also through the induction of DNA damage (78,79).…”

Section: Er Stress and Autophagymentioning

confidence: 97%

Crosstalk between autophagy and intracellular radiation response (Review)

Wang

Huang

et al. 2016

International Journal of Oncology

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Abstract. Autophagy induced by radiation is critical to cell fate decision. Evidence now sheds light on the importance of autophagy induced by cancer radiotherapy. Traditional view considers radiation can directly or indirectly damage DNA which can activate DNA damage the repair signaling pathway, a large number of proteins participating in DNA damage repair signaling pathway such as p53, ATM, PARP1, FOXO3a, mTOR and SIRT1 involved in autophagy regulation. However, emerging recent evidence suggests radiation can also cause injury to extranuclear targets such as plasma membrane, mitochondria and endoplasmic reticulum (ER) and induce accumulation of ceramide, ROS, and Ca 2+ concentration which activate many signaling pathways to modulate autophagy. Herein we review the role of autophagy in radiation therapy and the potent intracellular autophagic triggers induced by radiation. We aim to provide a more theoretical basis of radiation-induced autophagy, and provide novel targets for developing cytotoxic drugs to increase radiosensitivity. Contents1. Introduction 2. The role of autophagy in radiotherapy 3. DNA damage repair and autophagy 4. Mitochondrial damage and autophagy 5. ER stress and autophagy 6. ROS and autophagy 7. Ceramide and autophagy 8. Ca 2+ and autophagy 9. Targeting autophagy for radiotherapy 10. Conclusion IntroductionRadiotherapy is an effective strategy for the treatment of many kinds of cancer to kill or control the malignant tumor cells. However, its benefits have been limited due to radiation resistance. It is imperative to identify new targets and develop cytotoxic drugs to increase radiosensitivity. Radiosensitization has traditionally been performed with agents known to induce apoptosis. However, recent studies demonstrate autophagy induced by radiation also plays an important role in cancer Crosstalk between autophagy and intracellular radiation response (Review)

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“…46 In addition, recent results showed that both radiation and celecoxib could induce ER stress. 11,43,46 -48 Although the pharmacological actions of celecoxib that are responsible for inducing ER stress are considered to be involved in suppressing sarcoplasmatic/ER calcium ATPase activity, 48 -50 which is independent of a COX-2 inhibitory effect, 51 further analysis is required to establish this point.…”

Section: 38mentioning

confidence: 99%

Celecoxib enhances radiosensitivity of hypoxic glioblastoma cells through endoplasmic reticulum stress

et al. 2013

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Background. Refractoriness of glioblastoma multiforme (GBM) largely depends on its radioresistance. We investigated the radiosensitizing effects of celecoxib on GBM cell lines under both normoxic and hypoxic conditions. Methods. Two human GBM cell lines, U87MG and U251MG, and a mouse GBM cell line, GL261, were treated with celecoxib or g-irradiation either alone or in combination under normoxic and hypoxic conditions. Radiosensitizing effects were analyzed by clonogenic survival assays and cell growth assays and by assessing apoptosis and autophagy. Expression of apoptosis-, autophagy-, and endoplasmic reticulum (ER) stressrelated genes was analyzed by immunoblotting. Results. Celecoxib significantly enhanced the radiosensitivity of GBM cells under both normoxic and hypoxic conditions. In addition, combined treatment with celecoxib and g-irradiation induced marked autophagy, particularly in hypoxic cells. The mechanism underlying the radiosensitizing effect of celecoxib was determined to be ER stress loading on GBM cells. Conclusion. Celecoxib enhances the radiosensitivity of GBM cells by a mechanism that is different from cyclooxygenase-2 inhibition. Our results indicate that celecoxib may be a promising radiosensitizing drug for clinical use in patients with GBM. Keywords:autophagy, celecoxib, ER stress, glioblastoma, hypoxia, radiosensitivity. G lioblastoma multiforme (GBM) is the most frequently occurring malignant tumor of the central nervous system. 1 Despite standard carecomprising maximum surgical resection, 60 Gy of conventional radiotherapy, and chemotherapy with temozolomide (TMZ), the median survival time among patients with GBM is 1 year. 2The molecular mechanisms underlying the initiation and progression of GBM reported to date fall into 2 categories: (i) primary GBM with increased epidermal growth factor receptor (EGFR) expression and mutation of the phosphatase and tensin homolog and (ii) secondary GBM that is transformed from benign glioma types with stepwise mutations in the p53 and retinoblastoma genes. It is known that these genetic alterations in GBM are significantly associated with clinical prognosis.1 It has also been reported that methylation of O6-methylguanine-DNA methyltransferase increases the susceptibility of GBM tumor cells to alkylating agents, such as TMZ, 3 and mutation in the isocitrate dehydrogenase 1 gene was recently reported to significantly affect the prognosis in patients with GBM. 4 On the basis of these findings, therapy that targets these specific molecules could be a promising approach for controlling GBM. One possible target is cyclooxygenase-2 (COX-2) because a positive association has been reported among the levels of COX-2, EGFR/EGFRvIII, and activated signal transducer and activator of transcription 3 (STAT3).5 COX-2 expression was reportedly increased in human GBM and was negatively correlated with clinical outcomes in patients. 6 Celecoxib, a nonsteroidal anti-inflammatory drug (NSAID), selectively inhibits This drug is used clinically both for patients with ...

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ER stress induced by ionising radiation in IEC-6 cells

Abstract: Thus, we concluded that IR could induce moderate ER stress directly in IEC-6 cells.

Cited by 62 publications

References 25 publications

Radioprotective effects of genistein on HL-7702 cells via the inhibition of apoptosis and DNA damage

Radioprotective effects of genistein on HL-7702 cells via the inhibition of apoptosis and DNA damage

Crosstalk between autophagy and intracellular radiation response (Review)

Celecoxib enhances radiosensitivity of hypoxic glioblastoma cells through endoplasmic reticulum stress

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