scholarly journals Small interfering RNA targeting of Recepteur d'Origine Nantais induces apoptosis via modulation of nuclear factor-κB and Bcl-2 family in gastric cancer cells

2010 ◽  
Vol 24 (3) ◽  
Author(s):  
Jung
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Small Interfering Rna ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Gastric Cancer Cells ◽  
Rna Targeting ◽  
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 Functional p53 is required for triptolide-induced apoptosis and AP-1 and nuclear factor-κB activation in gastric cancer cells

Oncogene ◽  
2001 ◽  
Vol 20 (55) ◽  
pp. 8009-8018 ◽  
Author(s):  
Xiao-Hua Jiang ◽  
Benjamin Chun-Yu Wong ◽  
Marie Chia-Mi Lin ◽  
Geng-Hui Zhu ◽  
Hsiang-Fu Kung ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Nuclear Factor Κb ◽  
Nuclear Factor ◽  
Gastric Cancer Cells ◽  
Induced Apoptosis

scholarly journals Epithelial and Stromal Cells of Bovine Endometrium Have Roles in Innate Immunity and Initiate Inflammatory Responses to Bacterial Lipopeptides In Vitro via Toll-Like Receptors TLR2, TLR1, and TLR6

Endocrinology ◽  
2014 ◽  
Vol 155 (4) ◽  
pp. 1453-1465 ◽  
Author(s):  
Matthew L. Turner ◽  
James G. Cronin ◽  
Gareth D. Healey ◽  
Iain Martin Sheldon
Keyword(s):  
Stromal Cells ◽  
Small Interfering Rna ◽  
Inflammatory Responses ◽  
Nuclear Factor Κb ◽  
Cell Surface Receptor ◽  
Nuclear Factor ◽  
Endometrial Cells ◽  
Wide Range ◽  
Rna Targeting ◽  
Interfering Rna

Bacteria often infect the endometrium of cattle to cause endometritis, uterine disease, and infertility. Lipopeptides are commonly found among bacteria and are detected by the Toll-like receptor (TLR) cell surface receptor TLR2 on immune cells. Heterodimers of TLR2 with TLR1 or TLR6 activate MAPK and nuclear factor-κB intracellular signaling pathways to stimulate inflammatory responses. In the endometrium, epithelial and stromal cells are the first to encounter invading bacteria, so the present study explored whether endometrial cells can also mount inflammatory responses to bacterial lipopeptides via TLRs. The supernatants of pure populations of primary bovine endometrial epithelial and stromal cells accumulated the cytokine IL-6 and the chemokine IL-8 in response to triacylated or diacylated bacterial lipopeptides. The accumulation of IL-6 and IL-8 in response to triacylated lipopeptides was reduced by small interfering RNA targeting TLR2 or TLR1 but not TLR6, whereas cellular responses to diacylated lipopeptide were reduced by small interfering RNA targeting TLR2, TLR1, or TLR6. Both lipopeptides induced rapid phosphorylation of ERK1/2, p38, and nuclear factor-κB in endometrial cells, and inhibitors of ERK1/2 or p38 limited the accumulation of IL-6. The ovarian steroids estradiol and progesterone had little impact on inflammatory responses to lipopeptides. The endometrial epithelial and stromal cell responses to lipopeptides via TLR2, TLR1, and TLR6 provide a mechanism linking a wide range of bacterial infections to inflammation of the endometrium.

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.

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