LMP2A suppresses the role of AHR pathway through ERK signal pathway in EBV-associated gastric cancer

2021 ◽  
pp. 198399
Author(s):  
Yuanyuan Jiang ◽  
Hua Xiao ◽  
Lingling Sun ◽  
Yan Zhang ◽  
Shuzhen Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signal Pathway ◽  
Erk Signal Pathway

EBV down-regulates COX-2 expression via TRAF2 and ERK signal pathway in EBV-associated gastric cancer

2019 ◽  
Vol 272 ◽  
pp. 197735
Author(s):  
Yi-Fan Qi ◽  
Mengyang Liu ◽  
Yan Zhang ◽  
Wen Liu ◽  
Hua Xiao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signal Pathway ◽  
Cox 2 ◽  
Erk Signal Pathway

scholarly journals AnnexinA5 Might Suppress the Phenotype of Human Gastric Cancer Cells via ERK Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Xiaojie Wang ◽  
Yarui Dai ◽  
Yina Zhao ◽  
Meichuan Li ◽  
Jialu Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Signal Pathway ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Proliferation And Metastasis ◽  
Erk Signal Pathway ◽  
Apoptosis And Necrosis ◽  
Cell Proliferation And Metastasis

Gastric cancer is one of the most fatal diseases around the world. However, the mechanism of the development of gastric cancer is still not clarified. In addition, the anticancer drugs have cytotoxicity with different degrees. AnnexinA5, a member of the annexin family, has a great binding ability with the membrane phospholipid in a calcium dependent manner and is involved in the development of various cancers. This study aims to explore the influence of annexinA5 on human gastric cancer cells and whether it has the potential to be an auxiliary treatment to gastric cancer. In this study, the role of annexinA5 was detected from both the endogenous and the exogenous aspects on the gastric cancer cell lines MGC-803 and MKN-45. The cells were divided into a knockdown group in which RNA interference technique was used to suppress annexinA5 expression and a protein-supplementing group in which annexinA5 protein was added in the culture supernatant. After the suppression ratio of RNA interference was determined and the IC50 of annexinA5 protein was decided respectively, the cells’ proliferation was detected by MTT assay, colony formation assay, and the expression of PCNA. FCM assay and PI staining methods were applied to test cell apoptosis and necrosis. To investigate whether ANXA5 influence cell metastasis, wound healing assay and transwell assay were employed. To further detect the mechanism of annexinA5 action, the signal pathway was examined with Western Blot method. When ANXA5 gene was knocked down, cell proliferation and metastasis were promoted, while cell apoptosis was suppressed. On the other hand, after the annexinA5 protein was applied to the gastric cancer cells, cell proliferation and metastasis were inhibited, while cell apoptosis and necrosis were promoted. AnnexinA5 played its role via ERK signal pathway. ANXA5 acted as tumor suppressor gene in the gastric cancer by suppressing ERK signal pathway and has the potentiality to be an auxiliary anticancer agent.

scholarly journals The role of TNFAIP8-mediated mTOR-Akt-ULK1 signaling pathway in gastric cancer

2020 ◽  
Author(s):  
Zheng Chen ◽  
Jianguo Zhang ◽  
Chenyang Dong ◽  
Dongsheng Li ◽  
Yuehan Yin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Invasion ◽  
Signal Pathway ◽  
Gastric Cancer Cells ◽  
Mrna And Protein Expression ◽  
Gastric Cancer Cell Lines ◽  
A Cell

Abstract Background: The purpose of this article was to study the role of TNFAIP8 in gastric cancer. Methods: RT-PCR was used to detect the expression of TNFAIP8 mRNA and protein level in normal gastric mucosa cells and four gastric cancer cell lines. TNFAIP8 was silenced or overexpressed in two cell lines, CCK-8 cell viability was used, transwell experiment was used to detect cell invasion capability, and flow cytometry was used to detect cell apoptosis. TNFAIP was silenced or overexpressed in a cell line, and nude mice were inoculated to form transplanted tumors. HE staining and immunohistochemistry staining were used to detect the histopathological changes of tumors. Results: The mRNA and protein expression of TNFAIP8 was significantly up-regulated in GC patients and cells. After silencing and overexpressing TNFAIP8, gastric cancer cells with high expression increased, apoptosis decreased, and cell invasion increased. Expression of mTOR-Akt-ULK1 signal pathway was inhibited and autophagy signal was activated. Conclusions: Our findings indicate that TNFAIP8 inhibited gastric cancer cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy signal.

scholarly journals TNFAIP8 inhibits the proliferation of gastric cancer cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy

2020 ◽  
Author(s):  
Zheng Chen ◽  
Jianguo Zhang ◽  
Chenyang Dong ◽  
Dongsheng Li ◽  
Yuehan Yin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cell Invasion ◽  
Signal Pathway ◽  
Gastric Cancer Cells ◽  
Mrna And Protein Expression ◽  
Gastric Cancer Cell Lines ◽  
A Cell

Abstract Background : The purpose of this article was to study the role of TNFAIP8 in gastric cancer. Methods : RT-PCR was used to detect the expression of TNFAIP8 mRNA and protein level in normal gastric mucosa cells and four gastric cancer cell lines. TNFAIP8 was silenced or overexpressed in two cell lines, CCK-8 cell viability was used, transwell experiment was used to detect cell invasion capability, and flow cytometry was used to detect cell apoptosis. TNFAIP was silenced or overexpressed in a cell line, and nude mice were inoculated to form transplanted tumors. HE staining and immunohistochemistry staining were used to detect the histopathological changes of tumors. Results : The mRNA and protein expression of TNFAIP8 was significantly up-regulated in GC patients and cells. After silencing and overexpressing TNFAIP8, gastric cancer cells with high expression increased, apoptosis decreased, and cell invasion increased. Expression of mTOR-Akt-ULK1 signal pathway was inhibited and autophagy signal was activated. Conclusions : Our findings indicate that TNFAIP8 inhibited gastric cancer cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy signal.

scholarly journals TNFAIP8 inhibits gastric cancer proliferation by mTOR-Akt-ULK1 and autophagy signal pathway

2020 ◽  
Author(s):  
Zheng Chen ◽  
Jianguo Zhang ◽  
Chenyang Dong ◽  
Dongsheng Li ◽  
Yuehan Yin ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Lines ◽  
Cell Invasion ◽  
Signal Pathway ◽  
Rt Pcr ◽  
Transplanted Tumors ◽  
Cancer Proliferation ◽  
Mrna And Protein Expression ◽  
A Cell

Abstract Background: The purpose of this article was to study the role of TNFAIP8 in gastric cancer.Methods: RT-PCR was used to detect the expression of TNFAIP8 mRNA and protein level in normal gastric mucosa cells and four gastric cancer (GC) cell lines. TNFAIP8 was silenced or overexpressed in two cell lines, CCK-8 cell viability was used, transwell experiment was used to detect cell invasion capability, and flow cytometry was used to detect cell apoptosis. TNFAIP was silenced or overexpressed in a cell line, and nude mice were inoculated to form transplanted tumors. HE staining and immunohistochemistry staining were used to detect the histopathological changes of tumors. Results: The mRNA and protein expression of TNFAIP8 was significantly up-regulated in GC patients and cells. After silencing and overexpressing TNFAIP8, GC cells with high expression increased, apoptosis decreased, and cell invasion increased. Expression of mTOR-Akt-ULK1 signal pathway was inhibited and autophagy signal was activated. Conclusions: Our findings indicate that TNFAIP8 inhibited GC cells by inhibiting mTOR-Akt-ULK1 signal pathway and activating autophagy signal.

The role of cbl family of ubiquitin ligases in gastric cancer exosome-induced apoptosis of Jurkat T cells

2009 ◽  
pp. 1-8
Author(s):  
Jing-Lei Qu ◽  
Xiu-Juan Qu ◽  
Ming-Fang Zhao ◽  
Yue-E Teng ◽  
Ye Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
T Cells ◽  
Ubiquitin Ligases ◽  
Jurkat T Cells ◽  
Induced Apoptosis

Role of vitamin C in gastric cancer

2018 ◽  
Vol 01 (1) ◽  
Author(s):  
Takalkar U Vidyadhar
Keyword(s):  
Gastric Cancer ◽  
Vitamin C ◽  
Gastric Juice ◽  
Oxidative Dna Damage ◽  
Preventive Measure ◽  
Dietary Factors ◽  
Preventive Strategy ◽  
H Pylori

Gastric cancer is a multifactorial disease with complex interplay of environmental and genetic factors. Helicobacter pylori (H. pylori) infestation has been identified as the most important etiological agent in the pathogenesis of gastric cancer. Also, the role of dietary factors that is low consumption of fruits and vegetables have been found to be associated with gastric cancer. Among the dietary factors, antioxidants especially vitamin C has been found to confer the strongest protection against gastric cancer. Its anti-proliferative and pro-apoptotic action has been suggested in vitro. Because of its antioxidant activity, it protects cells against oxidative DNA damage caused by toxic effects of reactive oxygen species. It also inhibits production of carcinogenic N-nitroso compound in the stomach. The person with H. pylori infection has low levels of vitamin C in their gastric juice and levels of vitamin C normalizes on eradication of H. pylori. Vitamin C levels are high in gastric mucosa and gastric juice, sometimes more than that of in plasma. But gastric pathological conditions cause lowered secretion of vitamin C into gastric juice. Effect of H. pylori on vitamin C in gastric juice is reversible and on eradication of H. pylori, it returns to normal level. Hence, eradication of H. pylori and chemoprevention with antioxidant supplementation will be an effective preventive strategy to reduce the incidence of gastric cancer and related mortality. Vitamin C and gastric cancer is an area of potential interest for researchers as a preventive measure. Keywords: Vitamin C, H. pylori, gastric cancer.

Sign in / Sign up

Export Citation Format

Share Document