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

2017 ◽  
Vol 43 (1) ◽  
pp. 195-208 ◽  
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.

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

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
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.

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

2019 ◽  
Vol 18 ◽  
pp. 153303381987480 ◽  
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.

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

2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Yuming Zhang ◽  
Zhijun Mao ◽  
Fei Xue ◽  
Yu Zhang ◽  
Yuting Min ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Viability ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Migration And Invasion ◽  
Control Group ◽  
Human Gastric Cancer ◽  
Hoechst 33258 ◽  
Gastric Cancer Cells ◽  
Mtt Method

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.

scholarly journals m6A Methyltransferase 3 Promotes the Proliferation and Migration of Gastric Cancer Cells through the m6A Modification of YAP1

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Wenjie Zhou ◽  
Qingying Xian ◽  
Qi Wang ◽  
Chen Wu ◽  
Haijiao Yan ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines ◽  
Proliferation And Metastasis ◽  
And Migration ◽  
Proliferation And Migration

Gastric cancer is the most common gastrointestinal tumor with an increasing incidence. Furthermore, advanced gastric cancer is more common, but the mechanism underlying the proliferation and metastasis of gastric cancer has not been thoroughly explored. N6-methyladenosine (m6A) methyltransferase 3 (METTL3) may be involved in the proliferation and metastasis of gastric cancer. Therefore, Yes-associated protein 1 (YAP1) in the Hippo pathway was selected as the target, and the relationship between METTL3 and the proliferation and metastasis of gastric cancer was proved through a series of experiments. This research showed that the expression of m6A and METTL3 was upregulated in human gastric cancer tissues and gastric cancer cell lines. After lentiviral transfection, METTL3 silencing in AGS (human gastric adenocarcinoma cell line AGS) and MKN-45 (human gastric cancer cell line MKN-45) gastric cancer cell lines directly inhibited the proliferation, aggressiveness, and migration of gastric cancer cells. Mechanically, the inhibition of the YAP1-TEAD signaling pathway by peptide 17 reduces m6A methylation and the total mRNA level of YAP1. It also eliminates the promoting effect of METTL3 on the proliferation and migration of gastric cancer cells. In turn, the overexpression of YAP1 eliminates the inhibitory effect of METTL3 silencing on the proliferation, migration, and invasion of gastric cancer cells. This article proved that m6A methyltransferase METTL3 promoted the proliferation and migration of gastric cancer cells through the m6A modification of YAP1.

scholarly journals IFT80 Improves Invasion Ability in Gastric Cancer Cell Line via ift80/p75NGFR/MMP9 Signaling

2018 ◽  
Vol 19 (11) ◽  
pp. 3616 ◽  
Author(s):  
Rui Wang ◽  
Xiaoyan Deng ◽  
Chengfu Yuan ◽  
Hongmei Xin ◽  
Geli Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Reverse Transcription ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Quantitative Reverse Transcription Pcr ◽  
Reverse Transcription Pcr ◽  
Gastric Cancer Cell Lines

The assembly and maintenance of cilia depend on intraflagellar transport (IFT) proteins, which play an important role in development and homeostasis. IFT80 is a newly defined IFT protein and partial mutation of IFT80 in humans causes diseases such as Jeune asphyxiating thoracic dystrophy (JATD) and short rib polydactyly (SRP) type III, both characterized by abnormal skeletal development. However, the role and mechanism of IFT80 in the invasion of gastric cancer is unknown. We established SGC-7901 and MKN-45 gastric cancer cell lines that stably overexpressed IFT80, as verified by quantitative reverse transcription-PCR, Western blot, and immunofluorescence. Matrix metalloproteinase-9 (MMP9) plays an important role in tumor invasion, and its expression was assessed by quantitative reverse transcription-PCR, Western blotting, and immunofluorescence. The invasion ability of IFT80 on SGC-7901 and MKN-45 cells was examined by the Matrigel invasion assay. The relationship between p75NGFR, and the p75NGFR antagonists, PD90780 and IFT80, were detected by quantitative reverse transcription-PCR and Western blotting. We first detected an IFT80 expression pattern, and found that IFT80 was highly expressed in gastric cancer clinical samples. Overexpression of IFT80 in the gastric cancer cell lines, SGC-7901 and MKN-45, led to lengthening cilia. Additionally, overexpression of IFT80 significantly improved proliferation and invasion, but inhibited apoptosis, in gastric cancer cells. We further found that overexpression of IFT80 increased p75NGFR and MMP9 mRNA and protein expression. Treatment with the p75NGFR antagonist PD90780 inhibited the increased invasion ability resulting from overexpression of IFT80 in SGC-7901 and MKN-45 gastric cancer cells. Thus, these results suggest that IFT80 plays an important role in invasion of gastric cancer through regulating the ift80/p75NGFR/MMP9 signal pathways.

scholarly journals Anti-Cancer Effects of Radix Angelica Sinensis (Danggui) and N-Butylidenephthalide on Gastric Cancer: Implications for REDD1 Activation and mTOR Inhibition

2018 ◽  
Vol 48 (6) ◽  
pp. 2231-2246 ◽  
Author(s):  
Kuan-Fu Liao ◽  
Tsung-Lang Chiu ◽  
Sung-Ying Huang ◽  
Teng-Fu Hsieh ◽  
Shu-Fang Chang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Survival Rate ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Angelica Sinensis ◽  
Rna Seq ◽  
Gastric Cancer Cells ◽  
Mtor Inhibition

Background/Aims: Radix Angelica Sinensis (danggui in Chinese) is widely used in traditional chinese medicine (TCM). N-butylidenephthalide (BP), a bioactive compound in danggui, is a potential antitumor agent for various cancer types. However, its clinical effect and mechanism in the treatment of gastric cancer remain undetermined. Methods: The in vivo protective effect of danggui in patients with gastric cancer were validated using data from Taiwan’s National Health Insurance Research Database (NHIRD). The genes induced by BP-treatment were analyzed by whole transcriptome RNA sequencing (RNA-seq) and validated by real-time PCR, western blot and siRNA transfection. The effect of BP on AGS cell migration and invasion was evaluated in transwell assays. The antitumor effects of BP were evaluated in vivo in an AGS xenograft animal model. Results: Danggui users were found to have an increased survival rate when compared with danggui nonusers (log-rank test p = 0.002) . The use of danggui highly associated with decreased mortality (the adjusted hazard ratio (HR) of danggui user was 0.72 [95 % CI, 0.57-0.92] (p = 0.009). The in vitro results showed that BP inhibited gastric cancer cell proliferation, and triggered cellular apoptosis depending on the activation of mitochondrial apoptotic pathway. Using RNA-seq analysis we found that REDD1 was the highest transcript induced by BP in gastric cancer cells. BP induce an increase of REDD1 expression that inhibits mTOR signaling, thus inhibiting gastric cancer growth. We used RNA interference to demonstrate that the knock-down of REDD1 attenuated the BP-induced mTORC1 activation and growth inhibition. BP suppressed the growth of AGS xenografts tumor in vivo. Conclusion: Danggui can prolong the survival rate of gastric cancer patients in Taiwan. BP caused gastric cancer cell death through the activation of mitochondria-intrinsic pathway and induced the REDD1 expression leading to mTOR signal pathway inhibition in gastric cancer cells. BP inhibited the in vivo growth of AGS xenograft tumors. These results may provide the basis for a new therapeutic approach toward the treatment of gastric cancer progression.

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.

miR-3613 Regulates Gastric Cancer Cells Proliferation, Invasion, Migration and Apoptosis by Targeting Suppressor of Cytokine Signaling 4

2019 ◽  
Vol 9 (12) ◽  
pp. 1699-1705
Author(s):  
Yuming Luo ◽  
Wei Cao
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Western Blot ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Target Genes ◽  
Luciferase Reporter ◽  
Gastric Cancer Cells ◽  
And Migration

The present study aimed to investigate the effect of miR-3613 on the biological functions of gastric cancer cell lines. The expression of miR-3613 and SOCS4 in gastric cancer cells were detected by RT-qPCR and western blot. The target genes of miR-3613 were verified with the luciferase reporter system and western blot. The SOCS4 overexpression plasmid was constructed and transfected into gastric cancer cells. To further investigate the function of miR-3613, shRNA targeting miR-3613 and SOCS4 overexpression were transfected into SGC-7901. The growth of cells was detected by CCK-8, then the cell invasion and migration ability were detected by wound healing and transwell. Furthermore, the level of cell cycle was detected by flow cytometry. The expression of cell proliferation, cyclin and migration-related proteins were detected by western blot. The results revealed that the expression of miR-3613 is significantly increased in gastric cancer cells. SOCS4 is one of the target genes of miR-3613. Additionally, interference with miR-3613 promotes cell cycle arrest in gastric cancer cells and reversed the inhibitory effect of miR-3613 on biological function of gastric cells. Collectively, the data demonstrated that miR-3613 regulates gastric cancer cell by targeting SOCS4, which is expected to be an attractive target for the development of new drugs for the treatment of gastric cancer.

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