scholarly journals Identification ofGAS1as an Epirubicin Resistance-related Gene in Human Gastric Cancer Cells with a Partially Randomized Small Interfering RNA Library

2009 ◽  
Vol 284 (39) ◽  
pp. 26273-26285 ◽  
Author(s):  
Lina Zhao ◽  
Yanglin Pan ◽  
Yi Gang ◽  
Honghong Wang ◽  
Haifeng Jin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Human Gastric Cancer ◽  
Related Gene ◽  
Gastric Cancer Cells ◽  
Interfering Rna

scholarly journals Albendazole Exhibits Anti-Neoplastic Actions against Gastric Cancer Cells by Affecting STAT3 and STAT5 Activation by Pleiotropic Mechanism(s)

Biomedicines ◽  
2021 ◽  
Vol 9 (4) ◽  
pp. 362
Author(s):  
Min Hee Yang ◽  
In Jin Ha ◽  
Jae-Young Um ◽  
Kwang Seok Ahn
Keyword(s):  
Gastric Cancer ◽  
Reactive Oxygen Species ◽  
Transcription Factors ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Oxygen Species ◽  
Gastric Cancer Cells ◽  
Drug Induced ◽  
Cellular Apoptosis ◽  
Interfering Rna

Albendazole (ABZ) has been reported to display anti-tumoral actions against various maliganncies, but possible impact of ABZ on gastric cancer has not been deciphered. As aberrant phosphorylation of STAT3 and STAT5 proteins can regulate the growth and progression of gastric cancer, we postulated that ABZ may interrupt the activation of these oncogenic transcription factors. We found that ABZ exposure abrogated STAT3/5 activation, inhibited phosphorylation of Janus-activated kinases 1/2 and Src and enhanced the levels of SHP-1 protein. Silencing of SHP-1 gene by small interfering RNA (siRNA) reversed the ABZ-promoted attenuation of STAT3 as well as STAT5 activation and cellular apoptosis. In addition, these effects were noted to be driven by an augmented levels of reactive oxygen species caused by drug-induced GSH/GSSG imbalance. Thus, the data indicates that ABZ can modulate the activation of STAT3 and STAT5 by pleiotropic mechanisms in gastric cancer cells.

scholarly journals Inhibitory effect of survivin-targeting small interfering RNA on gastric cancer cells

2014 ◽  
Vol 13 (3) ◽  
pp. 6786-6803 ◽  
Author(s):  
Y.H. Li ◽  
M. Chen ◽  
M. Zhang ◽  
X.Q. Zhang ◽  
S. Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Inhibitory Effect ◽  
Gastric Cancer Cells ◽  
Interfering Rna

scholarly journals Interferon-αEnhances 5′-Deoxy-5-Fluorouridine-Induced Apoptosis by ERK-Dependant Upregulation of Thymidine Phosphorylase

2013 ◽  
Vol 2013 ◽  
pp. 1-8
Author(s):  
Yike Zhu ◽  
Ling Xu ◽  
Yibo Fan ◽  
Ce Li ◽  
Ye Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Thymidine Phosphorylase ◽  
Antitumor Efficacy ◽  
Erk Signaling ◽  
Gastric Cancer Cells ◽  
High Concentrations ◽  
Induced Apoptosis ◽  
Interfering Rna

5-Florouracil (5-FU) is the basic agent used in the treatment of gastric cancer. Capecitabine, a prodrug of 5-FU, displays increased antitumor efficacy compared with 5-FU in the clinic.5′-Deoxy-5-fluorouracil (5′-DFUR), the metabolite of capecitabine, is converted to 5-FU by the enzyme thymidine phosphorylase (TP), which is present at high concentrations in human tumors. In this study, we investigated the effect of interferon-α(IFN-α) on the sensitivity of gastric cancer cells to treatment with5′-DFUR and its relationship with TP expression. Preincubation of gastric cancer cells with IFN-αenhanced5′-DFUR-induced apoptosis via IFN-α-mediated upregulation of TP. The depletion of TP with small interfering RNA (siRNA) obviously inhibited IFN-α-induced upregulation of TP expression and thus prevented apoptosis induced by IFN-αand5′-DFUR. Treatment with IFN-αand combined IFN-αand5′-DFUR treatment were also associated with concomitant activation of ERK signaling. Treatment with the ERK inhibitor PD98059 or depletion of ERK with siRNA partially reversed IFN-α-induced upregulation of TP expression, thus partially preventing apoptosis induced by IFN-αand5′-DFUR. Taken together, our study shows that IFN-αenhanced5′-DFUR-induced apoptosis in gastric cancer cells by upregulation of TP expression, which is partially regulated by activation of ERK signaling.

scholarly journals Enhancement of Migration and Invasion of Gastric Cancer Cells by IQGAP3

Biomolecules ◽  
2020 ◽  
Vol 10 (8) ◽  
pp. 1194
Author(s):  
Natini Jinawath ◽  
Meng-Shin Shiao ◽  
Pichaya Chanpanitkitchote ◽  
Jisnuson Svasti ◽  
Yoichi Furukawa ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Leading Edge ◽  
Migration And Invasion ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Nih3t3 Cells ◽  
Common Causes ◽  
Dividing Cells ◽  
Interfering Rna

Although gastric cancer is one of the most common causes of cancer death in the world, mechanisms underlying this type of tumor have not been fully understood. In this study, we found that IQGAP3, a member of the IQGAP gene family, was significantly up-regulated in human gastric cancer starting from the early stages of tumor progression. Overexpression of IQGAP3 in 293T and NIH3T3 cells, which have no endogenous IQGAP3 expression, resulted in morphological change with multiple dendritic-like protrusions and enhanced migration. Overexpression of IQGAP3 also led to reduced cell–cell adhesion in 293T cells, likely as a result of its interactions with e-cadherin or β-catenin proteins. Additionally, IQGAP3 accumulated along the leading edge of migrating cells and at the cleavage furrow of dividing cells. In contrast, suppression of IQGAP3 by short-interfering RNA (siRNA) markedly reduced invasion and anchorage-independent growth of MKN1 and TMK-1 gastric cancer cells. We further confirmed that IQGAP3 interacted with Rho family GTPases, and had an important role in cytokinesis. Taken together, we demonstrated that IQGAP3 plays critical roles in migration and invasion of human gastric cancer cells, and regulates cytoskeletal remodeling, cell migration and adhesion. These findings may open a new avenue for the diagnosis and treatment of gastric cancer.

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