EBV-miR-BART12 inhibits cell migration and proliferation by targeting Snail expression in EBV-associated gastric cancer

Junctional adhesion molecule-like protein (JAML), a newly discovered junctional adhesion molecule (JAM), mediates the adhesion and migration processes of various immune cells and endothelial/epithelial cells, ultimately regulating inflammation reaction. However, its role in tumors remains to be determined. The expression of JAML was examined in gastric cancer (GC) and peritumoral tissues from 63 patients. The relationship between JAML expression and clinical characteristics was also observed. In vitro, GC cell migration and proliferation were assessed by wound healing assay, transwell migration assay and EdU incorporation assay. Immunohistochemical staining results showed that JAML expression level was higher in GC tissues than in peritumoral tissues. High expression of JAML in cancer tissues was associated with worse cell differentiation, local lymph node involvement, deep infiltration, and advanced stage. In vitro, we found that JAML silencing inhibited GC cell migration and proliferation, while JAML overexpression promoted GC cell migration and proliferation, partially via p38 signaling. Taken together, our study revealed a critical role for JAML to promote GC cell migration and proliferation. JAML might be a novel diagnostic biomarker and therapeutic target for GC.

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Visfatin facilitates gastric cancer malignancy by targeting snai1 via the NF-κB signaling

Human & Experimental Toxicology ◽

10.1177/09603271211006168 ◽

2021 ◽

pp. 096032712110061

Author(s):

D Cao ◽

L Chu ◽

Z Xu ◽

J Gong ◽

R Deng ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Migration ◽

Western Blot ◽

Blot Analysis ◽

Western Blot Analysis ◽

Epithelial Mesenchymal Transition ◽

Migration And Invasion ◽

Mesenchymal Transition ◽

Cell Migration And Invasion ◽

Protein Levels

Background: Visfatin acts as an oncogenic factor in numerous tumors through a variety of cellular processes. Visfatin has been revealed to promote cell migration and invasion in gastric cancer (GC). Snai1 is a well-known regulator of EMT process in cancers. However, the relationship between visfatin and snai1 in GC remains unclear. The current study aimed to explore the role of visfatin in GC. Methods: The RT-qPCR and western blot analysis were used to measure RNA and protein levels, respectively. The cell migration and invasion were tested by Trans-well assays and western blot analysis. Results: Visfatin showed upregulation in GC cells. Additionally, Visfatin with increasing concentration facilitated epithelial-mesenchymal transition (EMT) process by increasing E-cadherin and reducing N-cadherin and Vimentin protein levels in GC cells. Moreover, endogenous overexpression and knockdown of visfatin promoted and inhibited migratory and invasive abilities of GC cells, respectively. Then, we found that snai1 protein level was positively regulated by visfatin in GC cells. In addition, visfatin activated the NF-κB signaling to modulate snai1 protein expression. Furthermore, the silencing of snai1 counteracted the promotive impact of visfatin on cell migration, invasion and EMT process in GC. Conclusion: Visfatin facilitates cell migration, invasion and EMT process by targeting snai1 via the NF-κB signaling, which provides a potential insight for the treatment of GC.

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CDX2 and Reg IV expression and correlation in gastric cancer

BMC Gastroenterology ◽

10.1186/s12876-021-01678-9 ◽

2021 ◽

Vol 21 (1) ◽

Author(s):

Dandan Chai ◽

Huifen Du ◽

Kesheng Li ◽

Xueliang Zhang ◽

Xiaoqin Li ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Migration ◽

Cancer Cells ◽

Real Time ◽

Real Time Pcr ◽

Ectopic Expression ◽

Rank Correlation ◽

Migration And Invasion ◽

Gastric Cancer Cells ◽

Cell Migration And Invasion

Abstract Background Ectopic expression of CDX2 is associated with the development and progression of gastric cancer. Previous studies showed that CDX2 may be an upstream regulator of Reg IV expression in gastric cancer, and our previous report showed that Reg IV upregulated SOX9 expression and enhanced cell migration and invasion in gastric cancer cells. However, the regulatory roles of CDX2 have not been clarified in gastric cancer, and the correlation between CDX2 and Reg IV requires further study. Methods CDX2 and Reg IV were examined in gastric cancer specimens and paired adjacent tissues via real-time PCR and immunohistochemistry (IHC). The association between CDX2 and Reg IV was assessed using the χ2-test and Spearman’s rank correlation. To verify their relationship, knockdown and exogenous expression of CDX2 or Reg IV were performed in AGS and MKN-45 gastric cancer cells, and their expression was subsequently analyzed via a real-time PCR and western blotting. Wound-healing and Transwell assays were used to examine migration and invasion in AGS and MKN-45 cells following CDX2 silencing or overexpression. Results A positive correlation was observed between CDX2 and Reg IV expression at the mRNA and protein levels in gastric cancer tissues. CDX2 silencing significantly downregulated Reg IV expression, and CDX2 overexpression significantly upregulated Reg IV expression in AGS and MKN-45 cells. Neither Reg IV silencing nor overexpression had any effect on CDX2 protein expression in AGS or MKN-45 cells, even though both affected the expression of CDX2 mRNA. Functionally, CDX2 silencing significantly inhibited cell migration and invasion, and CDX2 overexpression significantly promoted cell migration and invasion in AGS and MKN-45 cells. Conclusions Our findings demonstrate that CDX2 expression was positively correlated with that of Reg IV in gastric cancer, and CDX2 promoted cell migration and invasion through upregulation of Reg IV expression in AGS and MKN-45 cells.

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Sevoflurane represses the migration and invasion of gastric cancer cells by regulating forkhead box protein 3

Journal of International Medical Research ◽

10.1177/03000605211005936 ◽

2021 ◽

Vol 49 (4) ◽

pp. 030006052110059

Author(s):

Fangfang Yong ◽

Hemei Wang ◽

Chao Li ◽

Huiqun Jia

Keyword(s):

Gastric Cancer ◽

Cell Migration ◽

Cancer Cells ◽

Cell Lines ◽

Migration And Invasion ◽

Control Group ◽

Gastric Cancer Cells ◽

Cell Migration And Invasion ◽

Forkhead Box ◽

Induced Apoptosis

Objective Previous studies suggested that sevoflurane exerts anti-proliferative, anti-migratory, and anti-invasive effects on cancer cells. To determine the role of sevoflurane on gastric cancer (GC) progression, we evaluated its effects on the proliferation, migration, and invasion of SGC7901, AGS, and MGC803 GC cells. Methods GC cells were exposed to different concentrations of sevoflurane (1.7, 3.4, or 5.1% v/v). Cell viability, migration, and invasion were evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and Transwell assays. Immunohistochemical staining and immunoblotting were performed to analyze forkhead box protein 3 (FOXP3) protein expression in tissue specimens and cell lines, respectively. Results FOXP3 was downregulated in human GC specimens and cell lines. Functionally, FOXP3 overexpression significantly inhibited the proliferation, migration, and invasion of GC cells and accelerated their apoptosis. Moreover, sevoflurane significantly blocked GC cell migration and invasion compared with the findings in the control group. However, FOXP3 silencing neutralized sevoflurane-induced apoptosis and the inhibition of GC cell migration and invasion. Sevoflurane-induced apoptosis and the suppression of migration and invasion might be associated with FOXP3 overactivation in GC cells. Conclusions Sevoflurane activated FOXP3 and prevented GC progression via inhibiting cell migration and invasion in vitro.

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Helicobacter pyloriinduces Snail expression through ROS-mediated activation of Erk and inactivation of GSK-3β in human gastric cancer cells

Molecular Carcinogenesis ◽

10.1002/mc.22464 ◽

2016 ◽

Vol 55 (12) ◽

pp. 2236-2246 ◽

Cited By ~ 11

Author(s):

Hoang-Kieu-Chi Ngo ◽

Hee Geum Lee ◽

Juan-Yu Piao ◽

Xiancai Zhong ◽

Ha-Na Lee ◽

...

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

Snail Expression ◽

Gsk 3Β

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H. pylori CagA activates the NLRP3 inflammasome to promote gastric cancer cell migration and invasion

Inflammation Research ◽

10.1007/s00011-021-01522-6 ◽

2021 ◽

Author(s):

XiaoYi Zhang ◽

Chao Li ◽

Dingyu Chen ◽

XiaoFeng He ◽

Yan Zhao ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Migration ◽

Cancer Cell ◽

Nlrp3 Inflammasome ◽

Gastric Cancer Cell ◽

Migration And Invasion ◽

Cancer Cell Migration ◽

Cell Migration And Invasion ◽

H Pylori

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The epigenetic silencing of LIMS2 in gastric cancer and its inhibitory effect on cell migration

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2006.08.128 ◽

2006 ◽

Vol 349 (3) ◽

pp. 1032-1040 ◽

Cited By ~ 30

Author(s):

Seung-Kyoon Kim ◽

Hae-Ran Jang ◽

Jeong-Hwan Kim ◽

Seung-Moo Noh ◽

Kyu-Sang Song ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Migration ◽

Inhibitory Effect ◽

Epigenetic Silencing

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Gonadotropin-induced ovarian cancer cell migration and proliferation require extracellular signal-regulated kinase 1/2 activation regulated by calcium and protein kinase Cδ

Endocrine Related Cancer ◽

10.1677/erc-09-0152 ◽

2010 ◽

Vol 17 (2) ◽

pp. 335-349 ◽

Cited By ~ 29

Author(s):

Inga Mertens-Walker ◽

Christine Bolitho ◽

Robert C Baxter ◽

Deborah J Marsh

Keyword(s):

Ovarian Cancer ◽

Cell Migration ◽

Protein Kinase ◽

Cancer Cell ◽

Ovarian Cancer Cell ◽

Cancer Cell Migration ◽

Extracellular Signal Regulated Kinase ◽

Extracellular Signal ◽

Gf 109203X ◽

Cell Migration And Proliferation

The gonadotropin hypothesis proposes that elevated serum gonadotropin levels may increase the risk of epithelial ovarian cancer (EOC). We have studied the effect of treating EOC cell lines (OV207 and OVCAR-3) with FSH or LH. Both gonadotropins activated the mitogen-activated protein kinase (MAPK)/extracellular signal-regulated kinase 1/2 (ERK1/2) pathway and increased cell migration that was inhibited by the MAPK 1 inhibitor PD98059. Both extra- and intracellular calcium ion signalling were implicated in gonadotropin-induced ERK1/2 activation as treatment with either the calcium chelator EGTA or an inhibitor of intracellular calcium release, dantrolene, inhibited gonadotropin-induced ERK1/2 activation. Verapamil was also inhibitory, indicating that gonadotropins activate calcium influx via L-type voltage-dependent calcium channels. The cAMP/protein kinase A (PKA) pathway was not involved in the mediation of gonadotropin action in these cells as gonadotropins did not increase intracellular cAMP formation and inhibition of PKA did not affect gonadotropin-induced phosphorylation of ERK1/2. Activation of ERK1/2 was inhibited by the protein kinase C (PKC) inhibitor GF 109203X as well as by the PKCδ inhibitor rottlerin, and downregulation of PKCδ was inhibited by small interfering RNA (siRNA), highlighting the importance of PKCδ in the gonadotropin signalling cascade. Furthermore, in addition to inhibition by PD98059, gonadotropin-induced ovarian cancer cell migration was also inhibited by verapamil, GF 109203X and rottlerin. Similarly, gonadotropin-induced proliferation was inhibited by PD98059, verapamil, GF 109203X and PKCδ siRNA. Taken together, these results demonstrate that gonadotropins induce both ovarian cancer cell migration and proliferation by activation of ERK1/2 signalling in a calcium- and PKCδ-dependent manner.

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Inferring parameters for a lattice-free model of cell migration and proliferation using experimental data

10.1101/186197 ◽

2017 ◽

Author(s):

Alexander P. Browning ◽

Scott W. McCue ◽

Rachelle N. Binny ◽

Michael J. Plank ◽

Esha T. Shah ◽

...

Keyword(s):

Experimental Data ◽

Cell Migration ◽

Spatial Clustering ◽

Cancer Cell Line ◽

Movement Direction ◽

Data Sets ◽

Collective Cell Migration ◽

Rejection Sampling ◽

Data Set ◽

Cell Migration And Proliferation

AbstractCollective cell spreading takes place in spatially continuous environments, yet it is often modelled using discrete lattice-based approaches. Here, we use data from a series of cell proliferation assays, with a prostate cancer cell line, to calibrate a spatially continuous individual based model (IBM) of collective cell migration and proliferation. The IBM explicitly accounts for crowding effects by modifying the rate of movement, direction of movement, and the rate of proliferation by accounting for pair-wise interactions. Taking a Bayesian approach we estimate the free parameters in the IBM using rejection sampling on three separate, independent experimental data sets. Since the posterior distributions for each experiment are similar, we perform simulations with parameters sampled from a new posterior distribution generated by combining the three data sets. To explore the predictive power of the calibrated IBM, we forecast the evolution of a fourth experimental data set. Overall, we show how to calibrate a lattice-free IBM to experimental data, and our work highlights the importance of interactions between individuals. Despite great care taken to distribute cells as uniformly as possible experimentally, we find evidence of significant spatial clustering over short distances, suggesting that standard mean-field models could be inappropriate.

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