The Mechanism of Safrole-Induced [Ca^(2+)]_i Rises and Non-Ca^(2+)-Triggered Cell Death in SCM1 Human Gastric Cancer Cells

2015 ◽  
Vol 預刊文章 (預刊文章) ◽  
pp. 1-10
Author(s):  
Tzu-Yi Hung 
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals Identification of a novel biomarker in tangeretin‑induced cell death in AGS human gastric cancer cells

2018 ◽  
Author(s):  
Silvia Yumnam ◽  
Suchismita Raha ◽  
Seong Kim ◽  
Venu Venkatarame Gowda Saralamma ◽  
Ho Lee ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

The role of transient receptor potential channel blockers in human gastric cancer cell viability

2012 ◽  
Vol 90 (2) ◽  
pp. 175-186 ◽  
Author(s):  
Byung Joo Kim ◽  
Sung-Young Kim ◽  
Sanghoon Lee ◽  
Ju-Hong Jeon ◽  
Hirofumi Matsui ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Growth And Survival ◽  
Lox Inhibitors ◽  
Transient Receptor

Transient receptor potential cation channel, subfamily M, receptor 7 (TRPM7) is a ubiquitous divalent-selective ion channel with its own kinase domain. Human gastric cancer cells express the TRPM7 channel, and the presence of this channel is essential for cell survival. Recent studies have suggested that 5-lipoxygenase (5-LOX) inhibitors are potent blockers of the TRPM7 channels. The aim of this study was to show the effects of 5-LOX inhibitors on the growth and survival of gastric cancer cells. Among 5-LOX inhibitors, nordihydroguaiaretic acid (NDGA), 2,3,5-trimethyl-6-(12-hydroxy-5,10-dodecadiynyl)-1,4-benzoquinone (AA861), and 3-[1-(p-chlorobenzyl)-5-(isopropyl)-3-tert-butylthioindol-2-yl]-2,2-dimethylpropanoic acid (MK886) were potent blockers of TRPM7-like currents in gastric cancer cells and also induced cell death. However, zileuton was ineffective in suppressing TRPM7-like current activity and inducing cell death. Moreover, a specific transient receptor potential cation channel, subfamily C, member 3 (TRPC3) inhibitor, a pyrazole compound (Pyr3), and a specific melastatin TRP (TRPM4) inhibitor, 9-phenanthrol, did not affect TRPM7-like currents or induce cell death. We conclude that TRPM7 has an important role in the growth and survival of gastric cancer cells and a likely potential target for the pharmacological treatment of gastric cancer.

scholarly journals Silencing of acetyl-CoA carboxylase-α gene in human gastric cancer cells inhibits proliferation via induction of apoptosis, autophagy and suppression of cell invasion

2021 ◽  
Vol 18 (10) ◽  
pp. 2025-2030
Author(s):  
Chunsong Yu ◽  
Xuehong Wu ◽  
Bihua Yao ◽  
Huaxing Tao
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Annexin V ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Acetyl Coa Carboxylase ◽  
Gastric Cancer Cells ◽  
Acetyl Coa

Purpose: To study the role and therapeutic potential of acetyl-CoA-carboxylase-α (ACC) in the management of gastric cancer. Methods: Expression of ACC in gastric cancer cell lines was determined using quantitative real-time polymerase chain reaction (qRT-PCR). Lipofectamine 2000 reagent was used for transfection, while cell viability was determined by MTT assay. Apoptotic cell death was assayed with 4′, 6-diamidino-2- phenylindole (DAPI) and acridine orange/ethidium bromide (AO/EB) staining. The proportion of apoptotic cells was estimated with Annexin V/PI staining. Wound healing and Transwell assays were employed to monitor cell migration and invasion, while protein expression was determined using western blotting. Results: The results showed that ACC was significantly enhanced in SNU-1 gastric cancer cells (4.2- fold). Silencing of ACC in SNU-1 gastric cancer cells caused significant decrease in cell proliferation (p < 0.05). Electron microscopy examination showed that ACC silencing triggered autophagic cell death in SNU-1 cells, and increased expression of LC3 II. Results from DAPI and AO/EB assays demonstrated that ACC silencing also promoted apoptosis in SNU-1 gastric cancer cells. Annexin V/PI assay results revealed that apoptotic cell population increased from 2.7 to 13.8 % due to ACC silencing (p < 0.05). Moreover, Bax expression increased, while Bcl-2 expression decreased upon ACC silencing. Transwell assay results indicate that ACC silencing caused marked decrease in the invasion of the SNU-1 cells and downregulation of the expressions of MMP-2 and MMP-9 (p < 0.05). Conclusion: ACC is likely to be an important therapeutic target for gastric cancer.

scholarly journals Inactivation of Akt by arsenic trioxide induces cell death via mitochondrial-mediated apoptotic signaling in SGC-7901 human gastric cancer cells

2014 ◽  
Vol 31 (4) ◽  
pp. 1645-1652 ◽  
Author(s):  
YAN-HUI GAO ◽  
HAO-PENG ZHANG ◽  
SHU-MENG YANG ◽  
YUE YANG ◽  
YU-YAN MA ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Arsenic Trioxide ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Apoptotic Signaling

Akebia saponin PA induces autophagic and apoptotic cell death in AGS human gastric cancer cells

2013 ◽  
Vol 59 ◽  
pp. 703-708 ◽  
Author(s):  
Mei-Ying Xu ◽  
Dong Hwa Lee ◽  
Eun Ji Joo ◽  
Kun Ho Son ◽  
Yeong Shik Kim
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals MHY218-induced apoptotic cell death is enhanced by the inhibition of autophagy in AGS human gastric cancer cells

2015 ◽  
Vol 47 (2) ◽  
pp. 563-572 ◽  
Author(s):  
PYOUNG RAK CHOI ◽  
YONG JUNG KANG ◽  
BOKYUNG SUNG ◽  
JAE HYUN KIM ◽  
HYUNG RYONG MOON ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Apoptotic Cell ◽  
Apoptotic Cell Death ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells

scholarly journals Comparative Proteomic Profiling of Tumor-Associated Proteins in Human Gastric Cancer Cells Treated with Pectolinarigenin

Nutrients ◽  
2018 ◽  
Vol 10 (11) ◽  
pp. 1596 ◽  
Author(s):  
Ho Jeong Lee ◽  
Venu Venkatarame Gowda Saralamma ◽  
Seong Min Kim ◽  
Sang Eun Ha ◽  
Preethi Vetrivel ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Death ◽  
Cancer Cells ◽  
Cell Lines ◽  
Proteomic Analysis ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Antitumor Effects ◽  
Aberrant Expression ◽  
Target Proteins

Pectolinarigenin (PEC), a natural flavonoid that is present in citrus fruits, has been reported to exhibit antitumor effects in several cancers. Though the mechanism of PEC-induced cytotoxicity effects has been documented, the proteomic changes that are associated with the cellular response to this flavonoid are poorly understood in gastric cancer cells. In this study, a comparative proteomic analysis was performed to identify proteins associated with PEC-induced cell death in two human gastric cancer cell lines: AGS and MKN-28. Two-dimensional gel electrophoresis (2-DE) revealed a total of 29 and 56 protein spots with significant alteration were screened in AGS and MKN-28 cells respectively. In total, 13 (AGS) and 39 (MKN28) proteins were successfully identified by mass spectrometry from the differential spots and they are known to be involved in signal transduction, apoptosis, transcription and translation, cell structural organization, and metabolism, as is consistent with multiple effects of PEC on tumor cells. Notably, novel target proteins like Probable ATP-dependent RNA helicase DDX4 (DDX4) and E3 ubiquitin-protein ligase LRSAM1 (LRSAM1) along with the commonly differential expressed proteins on both the cell lines that are treated with PEC were confirmed by immunoblotting. The DDX4 accelerates cell cycle progression by abrogating the G2 checkpoint when overexpressed in cancer cells, while the aberrant expression of LRSAM1 may be involved in the cancer pathology. Thus, proteomic analysis provides vital information about target proteins that are important for PEC-induced cell death in gastric cancer cells.

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