scholarly journals Resveratrol synergizes with cisplatin in antineoplastic effects against AGS gastric cancer cells by inducing endoplasmic reticulum stress‑mediated apoptosis and G2/M phase arrest

2020 ◽  
Author(s):  
Mengting Ren ◽  
Xinxin Zhou ◽  
Mengli Gu ◽  
Wenrui Jiao ◽  
Mosang Yu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Phase Arrest ◽  
M Phase

scholarly journals Blockade of TRPC6 channels induced G2/M phase arrest and suppressed growth in human gastric cancer cells

2009 ◽  
Vol 125 (10) ◽  
pp. 2281-2287 ◽  
Author(s):  
Rong Cai ◽  
Xia Ding ◽  
Kechun Zhou ◽  
Yu Shi ◽  
Ruiliang Ge ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Phase Arrest ◽  
M Phase

scholarly journals Casticin Potentiates TRAIL-Induced Apoptosis of Gastric Cancer Cells through Endoplasmic Reticulum Stress

PLoS ONE ◽  
2013 ◽  
Vol 8 (3) ◽  
pp. e58855 ◽  
Author(s):  
Yuan Zhou ◽  
Li Tian ◽  
Lingzhi Long ◽  
Meifang Quan ◽  
Fei Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Gastric Cancer Cells ◽  
Induced Apoptosis

OSU-03012 induces apoptosis of gastric cancer cells through endoplasmic reticulum stress triggered inhibition of Akt and STAT3 signaling pathways.

2020 ◽  
Vol 38 (15_suppl) ◽  
pp. e15630-e15630
Author(s):  
Wei Peng ◽  
Xia Xu ◽  
Xiaoxiang Chen ◽  
Jifeng Feng ◽  
Bo Shen ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Dependent Manner ◽  
Preclinical Development ◽  
Gastric Cancer Cells ◽  
Stat3 Signaling ◽  
Caspase Family

e15630 Background: As the chemotherapeutic resistance and postoperative relapse rates of gastric cancer rise year by year, searching for novel chemoprevention compounds has become fairly imminent. 2-amino-N-{4-[5-(2-phenanthrenyl)-3-(trifluoromethyl)-1H-pyrazol-1-yl]-phenyl} acetamide (OSU-03012), a derivative of anti-inflammatory drug celecoxib, has recently been shown to have anti-tumor effects. But its roles and underling mechanisms in gastric cancer is rather unknown. Methods: In this study, we show for the first time that OSU-03012 inhibits the growth and potently induces the apoptosis of gastric cancer cells in vitro in a time- and dose-dependent manner. Results: We demonstrate that OSU-03012 induces cell death through endoplasmic reticulum stress (ERS) mediated up-regulation of PTEN, sequentially followed by the suppression of Akt-STAT3 axis, the activation of the mitochondrial membrane protein Bim, mitochondrial damage and finally the release of the caspase family proteases. Conclusions: Our data provide evidences to support OSU-03012 as a potential therapeutic agent for gastric cancer, which may facilitate further preclinical development of anti-tumor drugs.

Effect of proton pump inhibitors on the occurrence and development of gastric cancer and the polarization of macrophages in the microenvironment to M2-type.

2020 ◽  
Vol 38 (4_suppl) ◽  
pp. 437-437
Author(s):  
Xiao-Qing Lu ◽  
Shengxiao Zhang ◽  
Huan-Hu Zhang
Keyword(s):  
Gastric Cancer ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Cancer Cells ◽  
Proton Pump Inhibitors ◽  
Proton Pump ◽  
Signal Pathways ◽  
Main Role ◽  
Gastric Cancer Cells ◽  
Cancer Tissues

437 Background: Long-term use of Proton pump inhibitors was associated with an increased gastric cancer(GC) risk in subjects even after HP eradication therapy. In contrast some basic research showed that PPI inhibited the growth of GC. In the tumor-microenvironment (TME), macrophages that are recruited around the tumor are activated to form the tumor-associated macrophages (TAMs), which are the most abundant mononuclear cells in the tumor infiltrating leukocytes. Many studies have shown that TAMs are associated with poor prognosis of tumors. Methods: Immunohistochemistry was used to detect the phenotype of macrophages in patients with gastric cancer treated with PPI or without PPI. Transcriptomics sequencing analyzed the signal pathways that were highly expressed in PPI-treated gastric cancer for further exploring the mechanism of PPI's main role in gastric cancer cells. In vitro, explore the effects of PPI on gastric cancer cells and the next step on macrophages. The effects of PPI on the growth of gastric cancer and the degree of infiltration and phenotype transformation of macrophages were verified by in vivo experiments. Results: In the gastric cancer tissues treated with PPI, the macrophage phenotype is mostly M2 type, thereby exerting a cancer promoting effects. Transcriptome results showed high expression of genes associated with endoplasmic reticulum stress in gastric cancer tissues after PPI treatment, compared with patients who were not treated with PPI. Among them, GRP78 is a classic marker of endoplasmic reticulum stress. It was not only highly expressed in gastric cancer treated by PPI, but also acted on macrophages through exosomes secreted by gastric cancer cells, and caused macrophage to polarize to M2. Conclusions: PPI caused GC cells to overexpress GRP78 which was secrete into the microenvironment through exosomes, thereby transforming macrophages into M2 type under the action of GRP78. Finally M2 type macrophages promoted the progression of gastric cancer.

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