scholarly journals Study on the Biological Characteristics of CD133+ Cells Interfered by RNA Interference in Gastric Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-11 ◽  
Author(s):  
Ji-wei Yu ◽  
Shou-lian Wang ◽  
Ju-gang Wu ◽  
Rui-qi Lu ◽  
Xiao-chun Ni ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Nude Mice ◽  
Interference Effect ◽  
Tumor Formation ◽  
Biological Characteristics ◽  
Control Group ◽  
Gastric Cancer Cells ◽  
Transplanted Tumor ◽  
Sphere Formation

Background. To detect the changes of biological characteristics in gastric cancer cells interfered by CD133-specific small interfering RNA (siRNA). Methods. First to select the siRNA which has the strongest interference effect among 3 siRNAs (i.e., siRNA1, siRNA2, and siRNA3) in KATO-III cells by RT-PCR and Western blotting assays. Then, CD133+ cells were sorted out from KATO-III cells using an immunomagnetic bead sorting method and transfected with the selected siRNA. Furthermore, the proliferating characteristics, the antichemotherapeutic assessment, Transwell invasion assay, monoclonal sphere formation assay, and subcutaneous transplanted tumor formation assay in nude mice were investigated. Results. siRNA3 showed the strongest interference effect in KATO-III cells. As compared to the uninterfered control group, the CD133+ cells treated by siRNA3 showed significant decreases in the abilities of proliferation, invasion, clone sphere formation, and resistance to antitumour drugs as well as the weight and size of the transplanted tumor, which was nearly similar to that of CD133− cells. Additionally, the protein expression level of the EMT factor E-cadherin increased while those of EMT-related Snail and N-cadherin decreased in CD133+ cells interfered by siRNA3. Conclusion. Inhibition of CD133 gene expression reduces the abilities of gastric cancer cells in proliferation, invasion, clonal sphere formation, and chemoresistance as well as tumor formation in nude mice.

scholarly journals Combination of ω-3 Polyunsaturated Fatty Acids with 5-FU Inhibits SGC7901 Gastric Cancer Cell Growth via Rho-ROCK1 Signaling Pathway in Nude Mice

2021 ◽  
Author(s):  
Jiang Yiyan ◽  
Wang Keke ◽  
Lou Zhefeng ◽  
Hong Dan ◽  
Min Tao
Keyword(s):  
Gastric Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Nude Mice ◽  
Protein Level ◽  
Combination Group ◽  
Control Group ◽  
Mrna Levels ◽  
Caspase 9 ◽  
Gastric Cancer Cells

Abstract Background: Gastric cancer is one of the most common malignancy with high mortality rate in the world. Systemic chemotherapy is thought to be an important treatment. However, due to the unsatisfactory efficiency and obvious side effects, it is urgent to detect new therapy strategy for gastric cancer. This study was aimed to investigate the effects and mechanisms of ω-3 polyunsaturated acids (PUFAs) combined with 5-FU on the growth of gastric cancer cells in nude mice. Methods: BALB/C nude mice were injected subcutaneously with SGC7901 gastric cancer cells to establish a tumor-bearing mouse model. The tumor growth in vivo was observed. Morphological of tumor specimens was observed by HE staining. The mRNA levels of RhoA, RhoC and ROCK1 in tumor tissues were detected by qPCR, and their protein levels were detected by immunofluorescence and Western Blot. Meanwhile, apoptosis –related proteins were also determined by Western Blot.Results: Compared with the NC control group, the tumor volume and weight in ω-3 PUFAs and 5-Fu groups were insignificantly lower, but significantly lower in the combination group. Compared with the abundant blood supply in the NC group, HE staining showed multifocal tumor necrosis in the three intervention groups, and this change was the most prominent in the combination group. And qPCR results showed that the mRNA levels of RhoA in the combination groups were significantly lower than this in the other groups. Immunofluorescence showed that the level of RhoA protein in the three intervention groups decline in varying degrees, especially in the combination group. Western Blot showed that the protein level of RhoA in the three intervention groups were significantly lower than those in the NC control group, especially in the combination group. Meanwhile, the protein level of ROCK1 in both 5-FU group and the combination group were significantly lower, especially in the combination group. Compared with the control group, the levels of Bcl-2 and Caspase-9 decreased in the combination group, the level of cleaved Parp was increased at the same time.Conclusion: ω-3 PUFAs combined with 5-FU may inhibit tumor growth through the Rho/ROCK pathway and promote apoptosis by down-regulating the levels of Bcl-2 and Caspase-9 and induce the increase of cleaved Parp level.

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

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.

scholarly journals Effects of siRNA-mediated silencing of Bmi-1 gene expression on proliferation of gastric cancer cells

2019 ◽  
Vol 17 ◽  
pp. 205873921984553
Author(s):  
Ying Guo ◽  
Li Zhang ◽  
Guangyu Zhou ◽  
Qingjie Ma ◽  
Shi Gao ◽  
...  
Keyword(s):  
Gene Expression ◽  
Gastric Cancer ◽  
Flow Cytometry ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Negative Control ◽  
Control Group ◽  
Gastric Cancer Cells ◽  
Ags Cells

This study was designed to investigate the effects of siRNA-mediated silencing of Bmi-1 gene expression on proliferation of AGS gastric cancer cell. siRNA Bmi-1 was transfected into human AGS gastric cancer cells by liposome (as siRNA Bmi-1 group) with negative control (as control group); the expressions of Bmi-1 and apoptosis-related genes like P21, Bax, and Bcl-2 in AGS cells were determined by Western blot method; the apoptosis of AGS cells was detected by flow cytometry double staining and Hoechst staining; and cell cycle was measured by flow cytometry. Compared with the control group, the expression of Bmi-1 in the siRNA Bmi-1 group was significantly decreased ( P < 0.05), the apoptosis rate was increased ( P < 0.05), and cell cycles were arrested at G1 phase (P < 0.05); the expression level of P21 and Bax in cells was significantly up-regulated while that of Bcl-2 down-regulated ( P < 0.05). The down regulation of Bmi-1 can inhibit the proliferation of AGS gastric cancer cell and promote its apoptosis, which takes such effects mainly by up-regulating P21 as well as Bax and down-regulating Bcl-2.

Compare the Effects of Magnolol on Gastric Cancer Cells Through c-Jun N-Terminal Kinase Signaling Pathway and Gold Magnetic

2021 ◽  
Vol 21 (2) ◽  
pp. 943-948
Author(s):  
Yu Chen ◽  
Xiuyun He ◽  
Dagang Feng ◽  
Shijie Li
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Cell Viability ◽  
Cancer Cells ◽  
Control Group ◽  
Magnetic Nanocomposites ◽  
Magnetic Composite ◽  
Composite Nanomaterials ◽  
Gastric Cancer Cells ◽  
Cell Proliferation Inhibition

This article explores the effects and mechanisms of magnolol on the proliferation of gastric cancer cells as well as the apoptosis. First, 0 (control group), 20, 40, and 80 /x mol/L magnolol were observed on SGC-7901 cells for 24, 48, and 72 h. We use MTT method to measure the cell viability, and apoptosis and cells were detected by flow cytometry. Cell proliferation inhibition rate, apoptosis and cell cycle experiments showed that P-value < 0.05 means the difference is statistically significant. And the results which compare the control group, the 20, 40, and 80 /x mol/L show that honokiol had lower cell viability (P < 0.01), increased apoptotic rate (P < 0.01), and cell cycle stay in the G1 phase (P < 0.01), so we found that honokiol may suppress the proliferation of SGC-7901 cells and stimulate apoptosis by regulating cyclin and apoptosis-related proteins. With the development of nanomaterials synthesis technology and application in biomedicine, gold magnetic composite nanomaterials have unique properties, so they have been widely concerned in many applications. We combine gold and magnetic nanomaterials through other nanostructures to achieve the integration of diagnosis and treatment of tumors. We have synthesized two kinds of gold magnetic nanocomposites, GNR-PPy-FA nanocomposites. With the role of chemotherapy and heat and light therapy, GNR-PPy-FA nanocomposites have high light-to-heat conversion efficiency. Cell experiments verify the effect of chemotherapy and photothermal treatment of composite nanomaterials. After incubation with gold magnetic composite nanomaterials, the cell survival rate of tumor cells decreased to about 15%. In addition, both types of gold magnetic nanocomposites have the ability to dually target cancer cells, and the modification of folic acid and cancer cell membranes makes the material more biocompatible.

scholarly journals Proliferin-related protein overexpression in SGC-7901 gastric cancer cells inhibits in vitro cell growth and tumorigenesis in nude mice

2013 ◽  
Vol 29 (6) ◽  
pp. 2243-2248 ◽  
Author(s):  
MIAO HE ◽  
LIMIN WANG ◽  
JUN PU ◽  
QIAOZHEN YANG ◽  
GANG LI ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Growth ◽  
Cancer Cells ◽  
Nude Mice ◽  
Related Protein ◽  
Protein Overexpression ◽  
Gastric Cancer Cells

scholarly journals Ethaselen synergizes with oxaliplatin in tumor growth inhibition by inducing ROS production and inhibiting TrxR1 activity in gastric cancer

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Haiyong Zhang ◽  
Jing Wu ◽  
Jinqiu Yuan ◽  
Huafu Li ◽  
Yawei Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Tumor Growth ◽  
Growth Inhibition ◽  
Cancer Cells ◽  
Nude Mice ◽  
Combined Treatment ◽  
Thioredoxin Reductase ◽  
Tumor Growth Inhibition ◽  
Gastric Cancer Cells

Abstract Background Oxaliplatin is one of the most commonly used chemotherapeutic agent for the treatment of various cancers, including gastric cancer. It has, however, a narrow therapeutic index due to its toxicity and the occurrence of drug resistance. Hence, it is of great significance to develop novel therapies to potentiate the anti-tumor effect and reduce the toxicity of oxaliplatin. In our previous study, we demonstrated that ethaselen (BBSKE), an inhibitor of thioredoxin reductase, effectively inhibited the growth of gastric cancer cells and promoted apoptosis in vitro. In the present study, we investigated whether BBSKE can potentiate the anti-tumor effect of oxaliplatin in gastric cancer in vivo and vitro. Methods Cellular apoptosis and ROS levels were analyzed by flow cytometry. Thioredoxin reductase 1 (TrxR1) activity in gastric cancer cells, organoid and tumor tissues was determined by using the endpoint insulin reduction assay. Western blot was used to analyze the expressions of the indicated proteins. Nude mice xenograft models were used to test the effects of BBSKE and oxaliplatin combinations on gastric cancer cell growth in vivo. In addition, we also used the combined treatment of BBSKE and oxaliplatin in three cases of gastric cancer Patient-Derived organoid (GC-PDO) to detect the anti-tumor effect. Results We found that BBSKE significantly enhanced oxaliplatin-induced growth inhibition in gastric cancer cells by inhibiting TrxR1 activity. Because of the inhibition of TrxR1 activity, BBSKE synergized with oxaliplatin to enhance the production of ROS and activate p38 and JNK signaling pathways which eventually induced apoptosis of gastric cancer cells. In vivo, we also found that BBSKE synergized with oxaliplatin to suppress the gastric cancer tumor growth in xenograft nude mice model, accompanied by the reduced TrxR1 activity. Remarkably, we found that BBSKE attenuated body weight loss evoked by oxaliplatin treatment. We also used three cases of GC-PDO and found that the combined treatment of BBSKE and oxaliplatin dramatically inhibited the growth and viability of GC-PDO with increased ROS level, decreased TrxR1 activity and enhanced apoptosis. Conclusions This study elucidates the underlying mechanisms of synergistic effect of BBSKE and oxaliplatin, and suggests that the combined treatment has potential value in gastric cancer therapy.

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