miRNA-195: The New Target of Inhibiting the Proliferation, Migration and Invasion of Gastric Cancer Cells via Propofol

Objective: To explore the effect of propofol (Prof) on the proliferation, migration and invasion of human gastric cancer cell MGC-803 and its molecular mechanism. Methods: The MTT method was used to study the effects of Prof with different doses and durations on the viability of MGC-803 cells. Hoechst 33258 staining and electron microscopy were used to detect the effects of Prof on MGC-803 cell apoptosis. Transwell experiments were used to detect the effects of Prof on the migration and invasion of MGC-803 cells. RT-PCR detects the effect of Prof on the expression of miR-195 in MGC-803 cells, and Western Blot detects the effect of Prof on the protein expression of JAK/STAT signaling pathway. Results: Compared with 0mg/ml Prof, 5mg/ml, 10mg/ml and 20mg/ml Prof treatment with 24h, 48h and 72h can significantly reduce cell viability (P <0.05). Compared with the Control group, the percentage of Hoechst 33258 staining positive cells in the Prof group and the apoptosis rate under the electron microscope were significantly increased (P <0.05). Compared with the Control group, the cell migration rate and invasion rate of the Prof group were significantly reduced (P <0.05). Compared with the Control group, the expression of miRNA-195 in the Prof group cells was increased significantly (P <0.05). Compared with the Control group, the activity of p-Jak1 and p-STAT3 proteins in the Prof group were significantly reduced (P <0.05). Conclusion: Prof can reduce the cell viability, migration and invasion of gastric cancer cell MGC-803, and promote its apoptosis. Its mechanism may be related to the promotion of miR-195 expression and inhibition of JAK/STAT signal pathway activity.

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A Comparative Proteomic Analysis of Erinacine A’s Inhibition of Gastric Cancer Cell Viability and Invasiveness

Cellular Physiology and Biochemistry ◽

10.1159/000480338 ◽

2017 ◽

Vol 43 (1) ◽

pp. 195-208 ◽

Cited By ~ 11

Author(s):

Hsing-Chun Kuo ◽

Yur-Ren Kuo ◽

Kam-Fai Lee ◽

Meng-Chiao Hsieh ◽

Cheng-Yi Huang ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Viability ◽

Cancer Cells ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Boyden Chamber ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

Induction Of Apoptosis ◽

Erinacine A

Background / Aims: Erinacine A, isolated from the ethanol extract of the Hericium erinaceus mycelium, has been demonstrated as a new alternative anticancer medicine. Drawing upon current research, this study presents an investigation of the molecular mechanism of erinacine A inhibition associated with gastric cancer cell growth. Methods: Cell viability was determined by Annexin V–FITC/propidium iodide staining and migration using a Boyden chamber assay to determine the effects of erinacine A treatment on the proliferation capacity and invasiveness of gastric cancer cells. A proteomic assay provided information that was used to identify the differentially-expressed proteins following erinacine A treatment, as well as the mechanism of its targets in the apoptotic induction of erinacine A. Results: Our results demonstrate that erinacine A treatment of TSGH 9201 cells increased cytotoxicity and the generation of reactive oxygen species (ROS), as well as decreased the invasiveness. Treatment of TSGH 9201 cells with erinacine A resulted in the activation of caspases and the expression of TRAIL. Erinacine A induction of apoptosis was accompanied by sustained phosphorylation of FAK/AKT/p70S6K and the PAK1 pathways, as well as the generation of ROS. Furthermore, the induction of apoptosis and anti-invasion properties by erinacine A could involve the differential expression of the 14-3-3 sigma protein (1433S) and microtubule-associated tumor suppressor candidate 2 (MTUS2), with the activation of the FAK/AKT/p70S6K and PAK1 signaling pathways. Conclusions: These results lead us to speculate that erinacine A may generate an apoptotic cascade in TSGH 9201 cells by activating the FAK/AKT/p70S6K/PAK1 pathway and upregulating proteins 1433S and MTUS2, providing a new mechanism underlying the anti-cancer effects of erinacine A in human gastric cancer cells.

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

European Journal of Inflammation ◽

10.1177/2058739219845534 ◽

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.

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circCOL1A1 Promotes the Progression of Gastric Cancer Cells through Sponging miR-145 to Enhance RABL3 Expression

Journal of Immunology Research ◽

10.1155/2021/6724854 ◽

2021 ◽

Vol 2021 ◽

pp. 1-20

Author(s):

Yue Ma ◽

Yanyi Ren ◽

Huitao Wen ◽

Chengcheng Cui

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Circular Rna ◽

Migration And Invasion ◽

Gastric Cancer Cells ◽

Gastric Cancer Cell Lines ◽

Microrna Sponge ◽

And Function

Circular RNA has been reported to be a new noncoding RNA which plays important roles in tumor progression. One of the most common functions of circular RNA is to regulate microRNA expression by acting as a microRNA sponge. However, the circular RNA expression profile and function remain mostly unclear in gastric cancer. In the study, we explored the expression and function of circCOL1A1 (hsa_circ_0044556) in gastric cancer. We performed RT-PCR with divergent primers, mRNA stability assay, and RNase R digestion assay to characterize circCOL1A1 in gastric cancer cell lines. qRT-PCR was applied to detect the level of circCOL1A1 in both gastric cancer cell lines and tissues. Gain- and loss-of-function studies were carried out to detect the influence of circCOL1A1 on gastric cancer cells by performing CCK8, migration, and invasion assays. The regulation of the downstream genes was identified by qRT-PCR, western blot assay, dual luciferase assay, and RNA pull-down assay. The results showed that circCOL1A1 was highly expressed in both gastric cancer cells and tissues. Silence of circCOL1A1 inhibited the proliferation, migration, and invasion of gastric cancer cells. circCOL1A1 regulated the expression of miR-145 by acting as a microRNA sponge, and the influence of circCOL1A1 could be abrogated by miR-145 mimics. Our research shows that miR-145 plays its functions through targeting and regulating RABL3. Inhibition of circCOL1A1/miR-145/RABL3 could effectively suppress gastric cancer cell proliferation, migration, and invasion. circCOL1A1 also promote the transformation of M1 into M2 macrophage. Our study identified circCOL1A1 as a novel oncogenic circRNA and will provide more information for gastric cancer therapy.

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DAB2IP Downregulation Enhances the Proliferation and Metastasis of Human Gastric Cancer Cells by Derepressing the ERK1/2 Pathway

Gastroenterology Research and Practice ◽

10.1155/2018/2968252 ◽

2018 ◽

Vol 2018 ◽

pp. 1-10 ◽

Cited By ~ 6

Author(s):

Liang Sun ◽

Yizhou Yao ◽

Ting Lu ◽

Zengfu Shang ◽

Shenghua Zhan ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Growth ◽

Cancer Cells ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

Cancer Cell Growth ◽

Normal Tissues

DAB2IP (DOC2/DAB2 interactive protein) is downregulated in several cancer types, and its downregulation is involved in tumor cell proliferation, apoptosis, metastasis, and epithelial-mesenchymal transition (EMT). We aimed to investigate the potential role of DAB2IP in the development and progression of gastric cancer. DAB2IP levels were analyzed in human gastric cancer and adjacent normal tissues by Western blots and immunohistochemistry. Potential roles of DAB2IP in regulating gastric cancer cell growth and metastasis were examined by genetic manipulation in vitro. The molecular signaling was determined to understand the mechanisms of observed DAB2IP effects. DAB2IP level is lower in gastric cancer tissues as compared to paired normal tissues. Knockdown of DAB2IP enhanced gastric cancer cell growth and metastasis in vitro and promoted EMT progress at both protein and mRNA levels. Silencing DAB2IP activated extracellular signal-regulated kinase 1/2 (ERK1/2) pathway, and the enhanced proliferation and migration ability induced by DAB2IP knockdown were reduced after incubation with U0126 in SGC7901 gastric cancer cells. Inhibition of DAB2IP enhances gastric cancer cell growth and metastasis through targeting the ERK1/2 signaling, indicating that it may serve as a potential target for treatment of gastric cancer.

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Circ_0000190 favors gastric cancer patients potentially via inhibiting miR-1252/PAK3 pathway

10.21203/rs.3.rs-29489/v1 ◽

2020 ◽

Author(s):

Gui Jun Wang ◽

Tian Yu Yu ◽

Yan Rong Li ◽

Yang Jun Liu ◽

Bei-Bei Deng

Keyword(s):

Gastric Cancer ◽

Cell Viability ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Luciferase Reporter ◽

Circular Rnas ◽

Cancer Tissue ◽

Human Gastric Cancer ◽

Rt Pcr ◽

And Migration

Abstract Background Gastric cancer accounts for 8.3% of all cancer death and is demonstrated associated with aberrant circular RNAs (circRNAs) expressions.Circ_0000190 has been noted with prognostic role in gastric cancer. We aim to investigate the role and the underlying mechanism of circ_0000190 in gastric cancer.Methods Circ_0000190 expressions were examined in gastric cancer and adjacent normal tissues by RT-PCR. With gastric cancer cell lines, circ_0000190 expression was detected by FISH and RT-PCR. After forced expression, the role of the circRNA in gastric cancer cell viability, apoptosis, proliferation, cell cycle and migration was observed. The potential effector of circ_0000190 was predicted by computational screen and validated by luciferase reporter assay. The association of the effectors with circ_0000190’s effects above mentioned were examined. Mice model of human gastric cancer was established to observe the underlying mechanisms of circ_0000190.Results Circ_0000190 was down-regulated in gastric cancer tissue and cells, with a major location in cytoplasm. After transfection, circ_0000190 inhibited gastric cancer cell viability, proliferation and migration, and induced apoptosis and cycle, which was correlated with increased capase-3 and p27 expression, and decreased cyclinD expression. The circRNA was validated as a sponge of miR-1252, which directly targeted PAK3. The effects by circ_0000190 on the cellular processes above mentioned were blocked by miR-1252 mimics, and this was rescued after further overexpression of PAK3.Conclusions Our results revealed that circ_0000190 protected against gastric cancer, and this was via directly targeting miR-767-5p/PAK3 axis. Therefore, employing circ_0000190 might be a promising therapeutic strategy for treatment of gastric cancer.

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LP1 from Lentinula edodes C91-3 Induces Autophagy, Apoptosis and Reduces Metastasis in Human Gastric Cancer Cell Line SGC-7901

International Journal of Molecular Sciences ◽

10.3390/ijms19102986 ◽

2018 ◽

Vol 19 (10) ◽

pp. 2986 ◽

Cited By ~ 2

Author(s):

Samana Batool ◽

Thomson Joseph ◽

Mushraf Hussain ◽

Miza Vuai ◽

Kavish. Khinsar ◽

...

Keyword(s):

Gastric Cancer ◽

Cell Cycle ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Lentinula Edodes ◽

Gastric Cancer Cell Line ◽

Expression Level ◽

Cell Counting ◽

Migration And Invasion ◽

Human Gastric Cancer

Present study aimed to elucidate the anticancer effect and the possible molecular mechanism underlying the action of Latcripin 1 (LP1), from the mushroom Lentinula edodes strain C91-3 against gastric cancer cell lines SGC-7901 and BGC-823. Cell viability was measured by Cell Counting Kit-8 (CCK-8); morphological changes were observed by phase contrast microscope; autophagy was determined by transmission electron microscope and fluorescence microscope. Apoptosis and cell cycle were assessed by flow cytometer; wound-healing, transwell migration and invasion assays were performed to investigate the effect of LP1 on gastric cancer cell’s migration and invasion. Herein, we found that LP1 resulted in the induction of autophagy by the formation of autophagosomes and conversion of light chain 3 (LC3I into LC3II. LP1 up-regulated the expression level of autophagy-related gene (Atg7, Atg5, Atg12, Atg14) and Beclin1; increased and decreased the expression level of pro-apoptotic (Bax) and anti-apoptotic (Bcl-2) proteins respectively, along with the activation of Caspase-3. At lower-doses, LP1 have shown to arrest cells in the S phase of the cell cycle and decreased the expression level of matrix metalloproteinase MMP-2 and MMP-9. In addition, it has also been shown to regulate the phosphorylation of one of the most hampered gastric cancer pathway, that is, protein kinase B/mammalian target of rapamycin (Akt/mTOR) channel and resulted in cell death. These findings suggested LP1 as a potential natural anti-cancer agent, for exploring the gastric cancer therapies and as a contender for further in vitro and in vivo investigations.

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Gene-expression profiles related to a synergistic effect of taxane and suberoylanilide hydroxamic acid combination treatment in gastric cancer cells.

Journal of Clinical Oncology ◽

10.1200/jco.2011.29.4_suppl.50 ◽

2011 ◽

Vol 29 (4_suppl) ◽

pp. 50-50

Author(s):

H. Chang ◽

S. Y. Rha ◽

H. Jeung ◽

J. Ahn ◽

J. Jung ◽

...

Keyword(s):

Gene Expression ◽

Gastric Cancer ◽

Cell Lines ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Cancer Cell Lines ◽

Human Gastric Cancer ◽

Suberoylanilide Hydroxamic Acid ◽

Gastric Cancer Cells ◽

Gastric Cancer Cell Lines

50 Background: We evaluated the cytotoxic effects of combining of suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, with taxanes in human gastric cancer cell lines, and evaluated the pre-treatment difference of gene profile to identify genes that could potentially mediate the cytotoxic response. Methods: Twenty-five gastric cancer cell lines with 22K gene expression data were treated with SAHA and paclitaxel or docetaxel, and the synergistic interaction between the drugs was evaluated in vitro using the combination index (CI) method. We performed significance analysis of microarray (SAM) to identify chemosensitivity-related genes in gastric cancer cell lines that were concomitantly treated with SAHA and taxane. We generated a correlation-matrix between gene expression and CI values to identify genes whose expression correlated with a combined effect of taxanes and SAHA. Results: Taxane and SAHA combination had a synergistic cytotoxic effect against taxane-resistant gastric cancer cells. We selected 49 chemosensitivity-related genes, which were commonly identified in paclitaxel and docetaxel combined with SAHA, via SAM analysis. Among them, nine common genes (SLIT2, REEP2, EFEMP2, CDC42SE1, FSD1, POU1F1, ZNF79, ETNK1, and DOCK5) were extracted from the subsequent correlation-matrix analysis. Conclusions: Taxane and SAHA combination could be efficacious for the treatment of gastric cancer. The genes which were related with the synergistic response to taxane and SAHA could serve as surrogate biomarkers to predict the therapeutic response in gastric cancer patients. We are researching to determine the expression of the nine genes in malignant human gastric cancer tissue and to correlate them with clinical information. No significant financial relationships to disclose.

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Effects of Huaier Polysaccharide SP1 on Gastric Cancer Cell Proliferation, Apoptosis, Migration, and Invasion by Regulating TGF-β/SMAD Signaling Pathway

Advances in Polymer Technology ◽

10.1155/2020/8486039 ◽

2020 ◽

Vol 2020 ◽

pp. 1-7

Author(s):

Miaoliang Chen ◽

Ying Lu ◽

Ruili Zhang ◽

Tienan Bi ◽

Shenkang Zhou

Keyword(s):

Gastric Cancer ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Gastric Cancer Cell Line ◽

Cancer Cell Line ◽

Signal Pathway ◽

Migration And Invasion ◽

Dependent Manner ◽

Gastric Cancer Cells

Objective. To study the effects of Huaier polysaccharide SP1 on the proliferation, apoptosis, migration, and invasion of gastric cancer cell line MGC-803 and the underlying mechanism. Methods. MGC-803 cells were cultured in vitro and treated with SP1. The effects of SP1 on the proliferation, apoptosis, migration, and invasion of MGC-803 cells were detected by CCK-8 assay, flow cytometry analysis, and Transwell assay, respectively. Western blot and qRT-PCR were used to detect the expression of related genes. Results. Our study showed that Huaier polysaccharide SP1 could inhibit proliferation, migration, invasion, and promote the apoptosis of MGC-803 cells in vitro in a dose-dependent manner. Huaier polysaccharide SP1 could inhibit the activation of TGF-β/SMAD signal pathway by upregulating SMAD7 expression, thereby downregulating the expression of SOX4, ZEB2, MMP9, Snail, and Slug. Conclusion. Huaier polysaccharide SP1 can regulate the proliferation, apoptosis, migration, and invasion of gastric cancer cells by promoting the expression of SMAD7 and inhibiting the activation of TGF-β/SMAD signal pathway as well as the expression of the downstream oncogenes.

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Influence of miR-376c-3p/SYF2 Axis on the Progression of Gastric Cancer

Technology in Cancer Research & Treatment ◽

10.1177/1533033819874808 ◽

2019 ◽

Vol 18 ◽

pp. 153303381987480 ◽

Cited By ~ 1

Author(s):

Bin Liu ◽

Guangchun Li ◽

Zhen Zhang ◽

Honglei Wu

Keyword(s):

Gastric Cancer ◽

Cancer Cells ◽

Cancer Cell ◽

Gastric Cancer Cell ◽

Quantitative Polymerase Chain Reaction ◽

Biological Significance ◽

Human Gastric Cancer ◽

Gastric Cancer Cells ◽

And Migration ◽

Proliferation And Migration

MicroRNA-376c-3p was previous reported to have a crucial role in the progression of human cancer. This study was aimed to investigate the influence of microRNA-376c-3p on the proliferation and migration of human gastric cancer cells and the associated mechanism. We explored the expression of microRNA-376c-3p in gastric cancer cells using reverse transcription-quantitative polymerase chain reaction. Also, we analyzed the association and biological significance of microRNA-376c-3p and SYF2 pre-mRNA-splicing factor in gastric cancer. MicroRNA-376c-3p expression was found downregulated in gastric cancer cell lines compared to the normal cell line. MicroRNA-376c-3p directly targeted SYF2 and reduced SYF2 expression. Overexpression of microRNA-376c-3p inhibits gastric cancer cell proliferation and migration. Besides that, overexpression of SYF2 abrogates the inhibitory influences on gastric cancer cell behaviors caused by microRNA-376c-3p mimic. These results showed that microRNA-376c-3p inhibits the proliferation and migration of gastric cancer cells via targeting SYF2.

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