scholarly journals Activation of P2×7 Receptor Promotes the Invasion and Migration of Colon Cancer Cells via the STAT3 Signaling

2020 ◽  
Vol 8 ◽  
Author(s):  
Wen-jun Zhang ◽  
Ce-gui Hu ◽  
Hong-liang Luo ◽  
Zheng-ming Zhu
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Receptor Activation ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Stat3 Pathway ◽  
Invasion And Migration ◽  
Sw480 Cells ◽  
And Migration

The pathological mechanism of colon cancer is very complicated. Therefore, exploring the molecular basis of the pathogenesis of colon cancer and finding a new therapeutic target has become an urgent problem to be solved in the treatment of colon cancer. ATP plays an important role in regulating the progression of tumor cells. P2 × 7 belongs to ATP ion channel receptor, which is involved in the progression of tumors. In this study, we explored the effect and molecular mechanism of ATP-mediated P2 × 7 receptor on the migration and metastasis of colon cancer cells. The results showed that ATP and BzATP significantly increased the inward current and intracellular calcium concentration of LOVO and SW480 cells, while the use of antagonists (A438079 and AZD9056) could reverse the above phenomenon. We found that ATP promoted the migration and invasion of LOVO and SW480 cells and is dose-dependent on ATP concentration (100–300 μM). Similarly, BzATP (10, 50, and 100 μM) also significantly promoted the migration and invasion of colon cancer cells in a concentration-dependent manner. While P2 × 7 receptor antagonists [A438079 (10 μM), AZD9056 (10 μM)] or P2 × 7 siRNA could significantly inhibit ATP-induced colon cancer cell migration and invasion. Moreover, in vivo experiments showed that ATP-induced activation of P2 × 7 receptor promoted the growth of tumors. Furthermore, P2 × 7 receptor activation down-regulated E-cadherin protein expression and up-regulated MMP-2 mRNA and concentration levels. Knocking down the expression of P2 × 7 receptor could significantly inhibit the increase in the expression of N-cadherin, Vimentin, Zeb1, and Snail induced by ATP. In addition, ATP time-dependently induced the activation of STAT3 via the P2 × 7 receptor, and the STAT3 pathway was required for the ATP-mediated invasion and migration. Our conclusion is that ATP-induced P2 × 7 receptor activation promotes the migration and invasion of colon cancer cells, possibly via the activation of STAT3 pathway. Therefore, the P2 × 7 receptor may be a potential target for the treatment of colon cancer.

scholarly journals INHBA promotes the proliferation, migration and invasion of colon cancer cells through the upregulation of VCAN

2021 ◽  
Vol 49 (6) ◽  
pp. 030006052110149
Author(s):  
Jia Guo ◽  
Yuan Liu
Keyword(s):  
Colon Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Cell Counting ◽  
Migration And Invasion ◽  
High Morbidity ◽  
Colon Cancer Cells ◽  
Invasion And Migration ◽  
And Migration ◽  
Cancer Tissues

Objective Colon cancer has high morbidity and mortality rates, and proliferation, invasion and migration play an important role in colon cancer progression. Here, the effects of inhibin subunit beta A (INHBA) on cell proliferation, invasion and migration were investigated. Methods The UALCAN database was used to assess INHBA expression in colon cancer tissues and predict the survival of patients with high and low INHBA expression. The relevant proteins were detected by RT-qPCR and western blot. Cell transfection was performed to overexpress or inhibit INHBA and versican (VCAN). The high correlation between INHBA and VCAN found through LinkedOmics and StarBase databases was verified by immunoprecipitation assays. Cell proliferation was detected by cell counting kit-8 and colony formation assays. Wound healing and Transwell assays were used to assess migration and invasion. Results INHBA expression was upregulated in colon cancer tissues and cells. INHBA inhibition impaired the proliferation, migration and invasion of these cells. In addition, we confirmed the correlation between INHBA and VCAN in colon cancer cells. Finally, we found that INHBA interference inhibited the aggressive behavior of colon cancer cells by downregulating VCAN. Conclusion INHBA promotes the proliferation, migration and invasion of colon cancer cells through the upregulation of VCAN.

scholarly journals Autumn Royal and Ribier Grape Juice Extracts Reduced Viability and Metastatic Potential of Colon Cancer Cells

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
Manuel Valenzuela ◽  
Lorena Bastias ◽  
Iván Montenegro ◽  
Enrique Werner ◽  
Alejandro Madrid ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Grape Juice ◽  
Metastatic Potential ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Gene Expressions ◽  
Anticancer Properties

Antioxidants are known to be beneficial to health. This paper evaluates the potential chemopreventive and anticancer properties of phenolic compounds present in grape juice extracts (GJE) from Autumn Royal and Ribier varieties. The effects of these GJE on viability (SRB day assay) and metastatic potential (migration and invasion parameters) of colon cancer cell lines HT-29 and SW-480 were evaluated. The effects of GJE on two matrix metalloproteinase gene expressions (MMP2 and MMP9) were also evaluated via qRT-PCR. In the former, GJE reduced cell viability in both cell lines in a dose-dependent manner. GJE treatment also reduced cell migration and invasion. Moreover, MMP-2 and MMP-9 gene expression diminished depending on extract and on cell type.Conclusions. These results provide novel information concerning anticancer properties of selected GJE by revealing selective cytotoxicity and the ability to reduce invasiveness of colon cancer cells.

Gypenosides inhibits migration and invasion of human oral cancer SAS cells through the inhibition of matrix metalloproteinase-2 -9 and urokinase-plasminogen by ERK1/2 and NF-kappa B signaling pathways

2010 ◽  
Vol 30 (5) ◽  
pp. 406-415 ◽  
Author(s):  
Kung-Wen Lu ◽  
Jung-Chou Chen ◽  
Tung-Yuan Lai ◽  
Jai-Sing Yang ◽  
Shu-Wen Weng ◽  
...  
Keyword(s):  
Oral Cancer ◽  
Matrix Metalloproteinase ◽  
Cancer Cells ◽  
Time Dependent ◽  
Migration And Invasion ◽  
Mrna Levels ◽  
Dependent Manner ◽  
Invasion And Migration ◽  
Oral Cancer Cells ◽  
And Migration

Gypenosides (Gyp), found in Gynostemma pentaphyllum Makino, has been used as a folk medicine in the Chinese population for centuries and is known to have diverse pharmacologic effects, including anti-proliferative and anti-cancer actions. However, the effects of Gyp on prevention from invasion and migration of oral cancer cells are still unsatisfactory. The purpose of this study was to investigate effects of Gyp treatment on migration and invasion of SAS human oral cancer cells. SAS cells were cultured in the presence of 90 and 180 μg/mL Gyp for 24 and 48 hours. Gyp induced cytotoxic effects and inhibited SAS cells migration and invasion in dose- and time-dependent response. Wound-healing assay and boyden chamber assay were carried out to investigate Gyp-inhibited migration and invasion of SAS cells. Gyp decreased the abundance of several proteins, including nuclear factor-kappa B (NF-κB), cyclooxygenase-2 (COX-2), extracellular signal-regulated kinase 1/2 (ERK1/ 2), matrix metalloproteinase-9, -2 (MMP-9, -2), sevenless homolog (SOS), Ras, urokinase-type plasminogen activator (uPA), focal adhesion kinase (FAK) and RAC-alpha serine/threonine-protein kinase (Akt), in a time-dependent manner. In addition, Gyp decreased mRNA levels of MMP-2, MMP-7, MMP-9 but did not affect FAK and Rho A mRNA levels in SAS cells. These results provide evidences for the role of Gyp as a potent anti-metastatic agent, which can markedly inhibit the metastatic and invasive capacity of oral cancer cells. The inhibition of NF-κB and MMP-2, -7 and -9 signaling may be one of the mechanisms that is present in Gyp-inhibited cancer cell invasion and migration.

scholarly journals The miR-200c/FUT4 axis prevents the proliferation of colon cancer cells by downregulating the Wnt/β-catenin pathway

2020 ◽  
Author(s):  
Jinchun Cong ◽  
Chuanjia Yang ◽  
Zhixiu Xia ◽  
Jian Gong ◽  
Hong Zhang
Keyword(s):  
Colon Cancer ◽  
Correlation Analysis ◽  
Cancer Cells ◽  
Pearson Correlation ◽  
Signalling Pathway ◽  
Migration And Invasion ◽  
Colon Cancer Cells ◽  
Pearson Correlation Analysis ◽  
Sw480 Cells ◽  
Related Proteins

Abstract BackgroundTo investigate the effects of miR-200c, which targets fucosyltransferase 4 (FUT4), on the proliferation, migration and invasion of colon cancer cells and to further explore its mechanism.MethodsWe assessed the miR-200c and FUT4 mRNA levels in LoVo and SW480 cells by quantitative real-time polymerase chain reaction (qRT-PCR), and their correlation was analysed by Pearson correlation analysis. LipofectamineTM 2000 transfection reagent was used to transfect miR-200c mimic, FUT4 siRNA, FUT4 mimic and FUT4 mimic negative control into LoVo and SW480 cells, and RT-PCR was used to analyse the transfection efficiency. Cell Counting Kit-8 (CCK-8), colony formation and transwell assays were used to detect the migration, invasion and proliferation of LoVo and SW480 cells. Immunofluorescence was used to analyse the expression of the Ki-67 protein. Moreover, the expression of Wnt/β-catenin signalling pathway-related proteins was detected by western blots. A double luciferase experiment was performed to verify the targeting relationship between miR-200c and FUT4. In vivo, tumour growth and Wnt/β-catenin signalling pathway-related proteins were also analysed. ResultsPearson correlation analysis showed that miR-200c and FUT4 were negatively correlated in LoVo and SW480 cells (correlation coefficients were -0.9046 and -0.9236, respectively). MiR-200c overexpression inhibited the proliferation, migration and invasion of LoVo cells by downregulating FUT4. The Ki67-positive cells and Wnt/β-catenin signalling pathway-related proteins were reduced in the miR-200c overexpression and FUT4 silencing groups. A bioinformatics analysis and a dual luciferase reporting system identified FUT4 as the target of miR-200c. ConclusionsIn conclusion, miR-200c overexpression inhibits FUT4 expression and downregulates the Wnt/β-catenin signalling pathway, thereby inhibiting the migration, invasion and proliferation of colon cancer cells.

scholarly journals Acetyl-11-Keto-Beta-Boswellic Acid Inhibits Cell Growth, Invasion, and Migration in Colon Cancer Cells by Modulating the Expression of MicroRNA Let-7 and the Mir-200 Family

2011 ◽  
Vol 140 (5) ◽  
pp. S-402-S-403 ◽  
Author(s):  
Masanobu Takahashi ◽  
Yan Shen ◽  
Alexander Link ◽  
Francesc Balaguer ◽  
C. Richard Boland ◽  
...  
Keyword(s):  
Colon Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Boswellic Acid ◽  
Colon Cancer Cells ◽  
Invasion And Migration ◽  
And Migration

scholarly journals 28-Hydroxy-3-oxoolean-12-en-29-oic Acid, a Triterpene Acid from Celastrus Orbiculatus Extract, Inhibits the Migration and Invasion of Human Gastric Cancer Cells In Vitro

Molecules ◽  
2019 ◽  
Vol 24 (19) ◽  
pp. 3513 ◽  
Author(s):  
Zewen Chu ◽  
Haibo Wang ◽  
Tengyang Ni ◽  
Li Tao ◽  
Liangliang Xiang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Invasion ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Celastrus Orbiculatus ◽  
Gastric Cancer Cells ◽  
Invasion And Migration ◽  
And Migration ◽  
Related Proteins

Gastric cancer is the fifth most common tumor and has the third-highest mortality rate among various malignant tumors, and the survival rate of patients is low. Celastrus orbiculatus extract has been shown to inhibit the activity of a variety of tumors. This study explored the inhibitory effect of the oleanane-type triterpenoid acid 28-hydroxy-3-oxoolean-12-en-29-oic acid molecule from Celastrus orbiculatus extract on gastric cancer cell invasion and metastasis and determined its mechanism. 28-Hydroxy-3-oxoolean-12-en-29-oic acid was first diluted to various concentrations and then used to treat SGC-7901 and BGC-823 cells. Cell proliferation was assessed by an MTT (thiazole blue) assay. Transwell and wound healing assays were used to assess cell invasion and migration. High-content imaging technology was used to further observe the effects of the drug on cell invasion and migration. Western blotting was used to assess the effects on the expression of matrix metalloproteinases (MMPs) and the effects on epithelial–mesenchymal transition (EMT)-related proteins and phosphorylation-related proteins. We found that 28-Hydroxy-3-oxoolean-12-en-29-oic acid inhibited the migration and invasion of SGC-7901 and BGC-823 gastric cancer cells in a dose-dependent manner. Consequently, 28-hydroxy-3-oxoolean-12-en-29-oic acid decreased the expression of EMT-related proteins and MMPs in gastric cancer cells and reduced protein phosphorylation, inhibiting the migration and invasion of gastric cancer cells.

scholarly journals Radixin Enhances Colon Cancer Cell Invasion by Increasing MMP-7 Production via Rac1-ERK Pathway

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Qi-Hong Jiang ◽  
Ai-Xiang Wang ◽  
Yan Chen
Keyword(s):  
Colon Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cell Invasion ◽  
Colon Cancer Cell ◽  
Erk Pathway ◽  
Colon Cancer Cells ◽  
Cancer Cell Invasion ◽  
Invasion And Migration ◽  
And Migration

As a member of the ezrin-radixin-moesin (ERM) family, radixin is overexpressed in many tumor tissues. However, little is known about its role in the progression of colon cancer. So we here aimed to determine the function of radixin in colon cancer cell invasion. Interestingly, we found that the expression of radixin was significantly elevated in colon cancer cells. Knockdown of radixin suppressed the invasion and migration of colon cancer cells. Further, knockdown of radixin inhibited the activation of Rac1 and ERK1/2, and decreased the expression and secretion of MMP-7. In addition, Rac1-ERK signaling pathway was required for the radixin-promoted invasion and MMP-7 production. Together, our findings suggest that radixin enhances the invasion and migration of colon cancer cells. Activation of Rac1-ERK pathway and consequent upregulation of MMP-7 production may contribute to the function of radixin in the regulation of colon cancer cell invasion. Thus, radixin may act as a novel target for the diagnosis and treatment of colon cancer.

Epigallocatechin-3-gallate inhibits proliferation and triggers apoptosis in colon cancer via the hedgehog/phosphoinositide 3-kinase pathways

2021 ◽  
Author(s):  
Feng Ding ◽  
Su Yang
Keyword(s):  
Colon Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Nude Mice ◽  
The Body ◽  
Antiproliferative Effect ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Colon Cancer Cells ◽  
Underlying Mechanisms

The present study evaluated whether EGCG effectively attenuates tumor growth in colon cancer cells and in the xenografts of nude mice and to investigated the underlying mechanisms by focusing on the Shh and PI3K pathways. Three kinds of colon cancer cells and BALB/c nude mice were used to evaluate the antiproliferative effect of EGCG.The results showed that EGCG exhibited an antiproliferative effect against colon cancer cells in a dose-dependent manner with low toxicity against normal colon epithelial cells. Administration of EGCG caused significant apoptosis and inhibited the migration and invasion of colon cancer cells. The toxic effect of EGCG was accompanied by downregulation of the Shh and PI3K/Akt pathways. In addition, EGCG reduced tumor weight without affecting the body weight of nude mice and inhibited the activation of the Shh and PI3K/Akt pathways in tumor tissue. Purmorphamine (Shh agonist) or IGF-1 (PI3K agonist) partly abolished the effect of EGCG on cell proliferation, migration and apoptosis. Cyclopamine (Shh inhibitor) and LY294002 (PI3K inhibitor) showed the similar toxic effects as EGCG on colon cancer cells. In conclusion, EGCG inhibited colon tumor growth via downregulation of the Shh and PI3K pathways and may be a potential chemotherapeutic agent against colon cancer.

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