Endoplasmic reticulum stress sensitizes human esophageal cancer cell to radiation

Pang, Xiaowu; He, Gang; Liu, Yangbo; Wang, Yan; Zhang, Bo

doi:10.3748/wjg.v19.i11.1736

Cited by 56 publications

(41 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…For example, cellular sensitivity to cisplatin was increased by the overexpression of GRP78, an abundant ER chaperon [32], or by treatment with tunicamycin, a chemical ER stress inducer [33]. Furthermore, cancer cells treated with acriflavin and also with tunicamycin have been reported to be sensitized to ionizing radiation through the activation of the UPR [34,35,36]. In the present study, GNG accumulated in cytoplasmic organelles and increased the expressions of several ER stress-related molecules such as IRE-1, suggesting that GNG acted as an ER stress inducer and enhanced X-ray-induced apoptosis.…”

Section: Discussionmentioning

confidence: 99%

Radiosensitization of tumor cells through endoplasmic reticulum stress induced by PEGylated nanogel containing gold nanoparticles

et al. 2014

View full text Add to dashboard Cite

High atomic number molecules, such as gold and platinum, are known to enhance the biological effect of X-irradiation. This study was aimed to determine the radiosensitizing potential of PEGylated nanogel containing gold nanoparticles (GNG) and the cellular mechanism involved. GNG pretreatment increased the levels of reproductive cell death and apoptosis induced by X-irradiation. GNG accumulated in cytoplasm and increased the expression of endoplasmic reticulum (ER) stress-related protein. GNG suppressed the repair capacity of DNA after X-irradiation by down-regulating DNA repair-related proteins. Our results suggest that GNG radiosensitized cells by enhancing apoptosis and impairing DNA repair capacity via ER stress induction.

show abstract

Section: Discussionmentioning

confidence: 99%

Radiosensitization of tumor cells through endoplasmic reticulum stress induced by PEGylated nanogel containing gold nanoparticles

et al. 2014

View full text Add to dashboard Cite

show abstract

“…After the cells were cultured adherent to wall for 24 h, the cell culture medium was discarded. Then 100 μL 5 ug/mL tunicamycin (Sigma-Aldrich Chemical Company, St Louis MO, USA) [53, 54] was added, and 3 repeated wells were arranged. Cells were cultured and observed for 24 h, followed by calculating cells survival rate in each group.…”

Section: Methodsmentioning

confidence: 99%

Activation of endoplasmic reticulum stress promotes autophagy and apoptosis and reverses chemoresistance of human small cell lung cancer cells by inhibiting the PI3K/AKT/mTOR signaling pathway

Fan

et al. 2016

Oncotarget

View full text Add to dashboard Cite

ObjectiveThis study aims to investigate the effects of endoplasmic reticulum stress (ERS) on autophagy, apoptosis and chemoresistance of human small cell lung cancer (SCLC) cells via the PI3K/AKT/mTOR signaling pathway.ResultsThe expressions of ERS-related proteins (PEAK, eIF2α and CHOP) up-regulated, autophagy-related proteins (LC3, LC3-II and Beclin1) and apoptosis-related proteins (Bax and procaspase-3) down-regulated in NCI-H446 and H69 cells after tunicamycin treatment for 24 h. Compared with the blank group, the tunicamycin, BEZ235 and tunicamycin + BEZ235 groups exhibited decreased expressions of p-PI3K, p-AKT and p-mTOR, and increased expressions of autophagy-related proteins (LC3, LC3-II and Beclin1) and apoptosis proteins (Bax and procaspase-3), and the most obvious changes were observed in the tunicamycin + BEZ235 group.Materials and MethodsCCK-8 assay was applied to select the best cell line from five SCLC cell lines (NCI-H446, H69, H526, H146 and H209). Finally, NCI-H446 and H69 cells were selected for further experiments. NCI-H446/CDDP and H69/CDDP were selected and divided into the blank group, tunicamycin (an ESR inducer) group, BEZ235 (inhibitors of PI3K/AKT/mTOR pathway) group and tunicamycin + BEZ235 group. Cell apoptosis was detected by flow cytometry. Autophagy was observed by fluorescence microscopy and flow cytometry. Western blotting was used to detect the expressions of ERS-related proteins, autophagy-related proteins, apoptosis-related proteins and PI3K/AKT/mTOR pathway-related proteins.ConclusionsOur findings provide evidence that the activation of ERS could promote autophagy and apoptosis and reverse chemoresistance of human SCLC cells by inhibiting the PI3K/AKT/mTOR pathway.

show abstract

“…PI3K/Akt signaling primarily exerts anti-apoptotic effects by affecting multiple downstream effector molecules (34). Knockout of PI3K, Akt and associated genes by genetic intervention, or inhibition by small molecule drugs, which blocks the activation of downstream anti-apoptotic effector molecules and promotes apoptosis, has become a key focus of research on cancer treatment (35).…”

Section: Discussionmentioning

confidence: 99%

Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways

et al. 2016

View full text Add to dashboard Cite

Abstract. Esophageal cancer is the most common gastrointestinal cancer. Psoralidin exhibits antioxidant, anti-apoptotic, anti-inflammatory and antitumor effects, which result in the inhibition of cancer formation. The present study aimed to investigate the effect of psoralidin on esophageal carcinoma proliferation and growth, and to elucidate its underlying mechanism of action. The effect of psoralidin on cell proliferation was investigated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium brom ide assay. Using a n a n nexin V-f luorescein isothiocyanate/propidium iodide apoptosis detection kit and 4' ,6-diamidino-2-phenylindole staining assay, the present study demonstrated that psoralidin significantly enhanced apoptosis of human esophageal carcinoma Eca9706 cells. In addition, caspase-3 activity was analyzed with a caspase-3 colorimetric assay kit, while nuclear factor (NF)-κB activity and protein phosphatidylinositol 3-kinase (PI3K)/Akt expression were measured with an NF-κB enzyme-linked immunosorbent assay kit and western blot analysis, respectively. Eca9706 cells were treated with a PI3K agonist in order to investigate the mechanism of action of psoralidin. It was observed that psoralidin was able to decrease the proliferation and promote the cellular apoptosis of Eca9706 cells in a dose-dependent manner. Furthermore, psoralidin was also able to inhibit the caspase-3 activity of Eca9706 cells in a dose-dependent manner. In addition, psoralidin inhibited NF-κB activity and reduced PI3K and Akt protein expression in Eca9706 cells. Notably, the PI3K agonist was able to reverse the effect of psoralidin on Eca9706 cells. The results of the present study demonstrated that psoralidin was able to inhibit proliferation and enhance apoptosis of human esophageal carcinoma cells via the NF-κB and PI3K/Akt signaling pathways.

show abstract

Endoplasmic reticulum stress sensitizes human esophageal cancer cell to radiation

Abstract: Our data showed that TM treatment sensitized human esophageal cancer cells to radiation via apoptosis and autophagy both in vitro and in vivo.

Cited by 56 publications

References 34 publications

Radiosensitization of tumor cells through endoplasmic reticulum stress induced by PEGylated nanogel containing gold nanoparticles

Radiosensitization of tumor cells through endoplasmic reticulum stress induced by PEGylated nanogel containing gold nanoparticles

Activation of endoplasmic reticulum stress promotes autophagy and apoptosis and reverses chemoresistance of human small cell lung cancer cells by inhibiting the PI3K/AKT/mTOR signaling pathway

Psoralidin inhibits proliferation and enhances apoptosis of human esophageal carcinoma cells via NF-κB and PI3K/Akt signaling pathways

Contact Info

Product

Resources

About