scholarly journals Gastrin/CCK-B Receptor Signaling Promotes Cell Invasion and Metastasis by Upregulating MMP-2 and VEGF Expression in Gastric Cancer

2022 ◽  
Vol 13 (1) ◽  
pp. 134-145
Author(s):  
Yan Zhao ◽  
Qinrong Wang ◽  
Yi Zeng ◽  
Yuan Xie ◽  
Jianjiang Zhou
Keyword(s):  
Gastric Cancer ◽  
Cell Invasion ◽  
Receptor Signaling ◽  
Invasion And Metastasis ◽  
Vegf Expression

RKIP expression associated with gastric cancer cell invasion and metastasis

Tumor Biology ◽  
2012 ◽  
Vol 33 (4) ◽  
pp. 919-925 ◽  
Author(s):  
Baoqing Jia ◽  
Hongyi Liu ◽  
Qinglong Kong ◽  
Bing Li
Keyword(s):  
Gastric Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Gastric Cancer Cell ◽  
Cancer Cell Invasion ◽  
Invasion And Metastasis

scholarly journals MicroRNA-940 promotes tumor cell invasion and metastasis by downregulating ZNF24 in gastric cancer

Oncotarget ◽  
2015 ◽  
Vol 6 (28) ◽  
pp. 25418-25428 ◽  
Author(s):  
Xinyang Liu ◽  
Xiaoxiao Ge ◽  
Zhe Zhang ◽  
Xiaowei Zhang ◽  
Jinjia Chang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Invasion And Metastasis

scholarly journals TRIM37 promotes cell invasion and metastasis by regulating SIP1-mediated epithelial–mesenchymal transition in gastric cancer

2018 ◽  
Vol Volume 11 ◽  
pp. 8803-8813 ◽  
Author(s):  
Dehu Chen ◽  
Xiaolan You ◽  
Yan Pan ◽  
Qinghong Liu ◽  
Gan Cao
Keyword(s):  
Gastric Cancer ◽  
Cell Invasion ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition

scholarly journals DDAH1 mediates gastric cancer cell invasion and metastasis via Wnt/β-catenin signaling pathway

2017 ◽  
Vol 11 (9) ◽  
pp. 1208-1224 ◽  
Author(s):  
Jianxin Ye ◽  
Jie Xu ◽  
Yun Li ◽  
Qiang Huang ◽  
Jinsheng Huang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Gastric Cancer Cell ◽  
Cancer Cell Invasion ◽  
Invasion And Metastasis

scholarly journals Galectin-1 From Cancer-Associated Fibroblasts Promotes the Invasion and Metastasis of Gastric Cancer Through TGF-β1-Induced Epithelial-Mesenchymal Transition

2021 ◽  
Author(s):  
xiaolan you ◽  
Jian Wu ◽  
Xiaojun Zhao ◽  
Xingyu Jiang ◽  
Wenxuan Tao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Invasion ◽  
Epithelial Mesenchymal Transition ◽  
Cancer Associated Fibroblasts ◽  
Invasion And Metastasis ◽  
Mesenchymal Transition ◽  
Invasion And Migration ◽  
And Migration ◽  
Tgf Β1

Abstract Background The gastric cancer (GC) microenvironment has important effects on biological behaviors, such as tumor cell invasion and metastasis. However, the mechanism by which the GC microenvironment promotes GC cell invasion and metastasis is unknown. The present study aimed to clarify the effects and mechanism of galectin-1 (GAL-1, encoded by LGALS1) on GC invasion and metastasis in the GC microenvironment.Methods The expression of GAL-1/ LGALS1 was determined using western blotting, immunohistochemistry, and quantitative real-time reverse transcription PCR in GC tissues. Besides, methods including stable transfection, Matrigel invasion and migration assays, and wound-healing assays in vitro; and metastasis assays in vivo, were also conducted.Results GAL-1 from cancer-associated fibroblasts (CAFs) induced the epithelial‑mesenchymal transition (EMT) of GC cells though the transforming growth factor beta (TGF-β1)/ Sma- and mad-related protein (Smad) pathway, and affected the prognosis of patients with GC. The level of GAL-1 was high in CAFs, and treating MGC-803 and SGC -7901 cell line with the conditioned medium from CAFs promoted their invasion and metastasis abilities. Overexpression of LGALS1 promoted the expression of TGF-β1 and induced EMT of GC cell lines. A TGF-β1 antagonist inhibited the invasion and migration of GC cells. In vivo, overexpression of LGALS1 promoted GC growth and metastasis, and the TGF-β1 antagonist dramatically reversed these events. Conclusions These findings suggested that high expression of GAL-1 in the GC microenvironment predicts a poor prognosis in patients with GC by promoting the migration and invasion of GC cells via EMT through the TGF-β1/Smad signaling pathway. The results might provide new therapeutic targets to treat GC.

Induction of MT1-MMP expression and enhancement of gastric cancer cells invasion by DARPP-32-CXCR4 interaction.

2013 ◽  
Vol 31 (4_suppl) ◽  
pp. 14-14
Author(s):  
Shoumin Zhu ◽  
Abbes Belkhiri ◽  
Wael El-Rifai
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Cancer Metastasis ◽  
Invasion Assay ◽  
Invasion And Metastasis ◽  
Gastric Cancer Cells ◽  
Ags Cells ◽  
Protein Levels

14 Background: Dopamine and cAMP-regulated phosphoprotein, Mr 32000 (DARPP-32) is amplified and overexpressed in approximately 70% of gastric cancers. The prognosis for gastric cancer patients remains poor, especially in more advanced stages. Recently, it was suggested that CXCL-12 and its receptor, CXCR4, are involved in gastric cancer metastasis. However, the detailed mechanism of gastric cancer metastasis is still not completely understood. Methods: Cells invasive activity was determined by invasion assay and HUVEC invasion assay. The association between DARPP-32 and CXCR4 was evaluated by immunofluorescence and co-immunoprecipitation assays. CXCR4 degradation was analyzed by Ubiquitination Assay. Results: Overexpression of DARPP-32 in AGS cells increased cell invasion with about as three-fold invasive cells as the vector control (p<0.01). As measured by HUVEC invasion assay, overexpression of DARPP-32 in AGS cells also had a significant increase in the invasive activity (p<0.001). We found that DARPP-32 led to increased CXCR4 and MT1-MMP protein levels in DARPP-32 expressing AGS cells. The co-immunoprecipitation and immunofluorescence experiments demonstrated the existence of DARPP-32 and CXCR4 in the same protein complex. AGS cells expressing DARPP-32 displayed stable protein levels of CXCR4. IP-Western blot showed reduced ubiquitination of CXCR4 protein following the overexpression of DARPP-32 and treatment with CXCL-12, as compared to controls. Using AMD3100 (0.2 ng/ml) overnight blocked DARPP-32-induced cell invasion. The knockdown of endogenous DARPP-32 by lentiviral DARPP-32 shRNA in MKN-45 cell line reversed these signaling effects and decreased cell invasive activity, as measured by invasion and HUVEC invasion Assay (p<0.01, p<0.05). Conclusions: The in vitro studies indicate that DARPP-32 plays a role in invasion and metastasis; DARPP-32 promotes invasion and metastasis of gastric cancer cells by interacted with CXCR4, delaying CXCL-12-induced CXCR4 Ubiquitination and blocking CXCR4 degradation, activating MMP2 by increasing MT1-MMP expression. The in vivo experiments are ongoing to determine the efficacy of DARPP-32 in mediating CXCR4 overexpression and metastasis.

scholarly journals KLF9 suppresses gastric cancer cell invasion and metastasis through transcriptional inhibition of MMP28

2019 ◽  
Vol 33 (7) ◽  
pp. 7915-7928 ◽  
Author(s):  
Yang Li ◽  
Qiang Sun ◽  
Mingchun Jiang ◽  
Shuang Li ◽  
Jiayu Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Gastric Cancer Cell ◽  
Cancer Cell Invasion ◽  
Invasion And Metastasis ◽  
Transcriptional Inhibition

MicroRNA-148a Suppresses Tumor Cell Invasion and Metastasis by Downregulating ROCK1 in Gastric Cancer

2011 ◽  
Vol 17 (24) ◽  
pp. 7574-7583 ◽  
Author(s):  
Biqiang Zheng ◽  
Linhui Liang ◽  
Chunmeng Wang ◽  
Shenglin Huang ◽  
Xi Cao ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Cell ◽  
Cell Invasion ◽  
Tumor Cell Invasion ◽  
Invasion And Metastasis
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