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 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 Hydrogen inhibits the proliferation and migration of gastric cancer cells by modulating lncRNA MALAT1/miR-124-3p/EZH2 axis

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Baocheng Zhu ◽  
Hengguan Cui ◽  
Weiqiang Xu
Keyword(s):  
Gastric Cancer ◽  
Tumor Growth ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Gastric Cancer Cells ◽  
Ezh2 Expression ◽  
Lncrna Malat1 ◽  
And Migration ◽  
Proliferation And Migration

Abstract Background Gastric cancer is one of the most prevalent and deadly malignancies without efficient treatment option. This study aimed to investigate the effect of hydrogen gas on the behavior of gastric cancer cells. Methods Gastric cancer cell lines MGC-803 and BGC-823 were treated with or without H2 /O2 gas mixture (66.7%:33.3% v/v). Proliferation and migration were assessed by MTT and scratch wound healing assays respectively. The expression of lncRNA MALAT1, miR-124-3p, and EZH2 was analyzed by real-time quantitative PCR and/or western blot. Tumor growth was estimated using xenograft mouse model. Results H2 gas significantly inhibited gastric tumor growth in vivo and the proliferation, migration, and lncRNA MALAT1 and EZH2 expression of gastric cancer cells while upregulated miR-124-3p expression. LncRNA MALAT1 overexpression abolished all the aforementioned effects of H2. LncRNA MALAT1 and miR-124-3p reciprocally inhibited the expression of each other. MiR-124-3p mimics abrogated lncRNA MALAT1 promoted EZH2 expression and gastric cancer cell proliferation and migration. Conclusions These data demonstrated that H2 might be developed as a therapeutics of gastric cancer and lncRNA MALAT1/miR-124-3p/EZH2 axis could be a target for intervention.

Overexpression of PIP5KL1 suppresses cell proliferation and migration in human gastric cancer cells

2009 ◽  
Vol 37 (5) ◽  
pp. 2189-2198 ◽  
Author(s):  
Lan Shi ◽  
Mei Zhao ◽  
Qing Luo ◽  
Yi-Ming Ma ◽  
Jia-Ling Zhong ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

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.

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.

scholarly journals Knockdown of hMex-3A by small RNA interference suppresses cell proliferation and migration in human gastric cancer cells

2012 ◽  
Vol 6 (3) ◽  
pp. 575-580 ◽  
Author(s):  
HONG JIANG ◽  
XUEMEI ZHANG ◽  
JINHONG LUO ◽  
CHUNYAN DONG ◽  
JUNLI XUE ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Rna Interference ◽  
Cancer Cells ◽  
Small Rna ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cell Proliferation And Migration ◽  
And Migration ◽  
Proliferation And Migration

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

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.

scholarly journals Exopolysaccharides from an Ophiopogon japonicus endophyte inhibit proliferation and migration in MC-4 human gastric cancer cells

2018 ◽  
Vol 7 (6) ◽  
pp. 1567-1576
Author(s):  
Wenjun Xu ◽  
Yongle Yang ◽  
Youguang Yang ◽  
Zhongxia Lu ◽  
Qunying Lu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Ophiopogon Japonicus ◽  
And Migration ◽  
Proliferation And Migration

Effect of p-PAQR3Thr32 on PD-L1 expression and immune evasion in gastric cancer.

2019 ◽  
Vol 37 (15_suppl) ◽  
pp. e15571-e15571
Author(s):  
Zhi-Qiang Ling
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Cancer Cell Lines ◽  
Expression Level ◽  
Gastric Cancer Cells ◽  
Gastric Cancer Cell Lines

e15571 Background: Therapies targeted to the immune checkpoint mediated by PD-1 and PD-L1 show antitumor activity in some solid tumors. We have now examined PD-L1 expression and its regulation in gastric cancer with p-PAQR3Thr32 protein. Methods: The expression of PD-L1 at the protein and mRNA levels in gastric cancer cell lines was examined by flow cytometry, real-time RT-PCR and western blot analysis, respectively. The expression of PD-L1 and p-PAQR3Thr32 protein in 319 surgically resected gastric cancer specimens was evaluated by immunohistochemical analysis. Results: The PD-L1 expression level was higher in gastric cancer cell lines positive for p-PAQR3Thr32 protein induced by glucose starvation than in those negative for the p-PAQR3Thr32 protein. Forced expression of p-PAQR3Thr32 protein in gastric cancer cells markedly increased PD-L1 expression, whereas endogenous PD-L1 expression in p-PAQR3Thr32 protein positive gastric cancer cells was attenuated by treatment with PAQR3 siRNAs. Furthermore, expression of PD-L1 was downregulated by inhibitors of the IRF1 and STAT1 in IFNs-PDL1 signaling pathway in gastric cancer cells positive for p-PAQR3Thr32 protein. At clinical tissue level, the expression level of PD-L1 was positively associated with the presence of p-PAQR3Thr32 protein in gastric cancer specimens. Moreover, the expression level of p-PAQR3Thr32 protein was negatively correlated with CD3, CD8, GZMA (CD8 T cell secretory factor) and positively correlated with CD68 (macrophage marker). Conclusions: Our findings that p-PAQR3Thr32 protein induced by glucose deficiency upregulate PD-L1 by activating IFNs-PDL1 signaling pathway in gastric cancer reveal a direct link between p-PAQR3Thr32 protein and PD-L1 expression. It is suggested that p-PAQR3Thr32 protein may be involved in tumor immunosuppression by inhibiting the proliferation and activity of CD8 T cells in gastric cancer tissues.

scholarly journals Myrrh induces the apoptosis and inhibits the proliferation and migration of gastric cancer cells through down-regulating cyclooxygenase-2 expression

2020 ◽  
Vol 40 (5) ◽  
Author(s):  
Mengxue Sun ◽  
Jie Hua ◽  
Gaoshuang Liu ◽  
Peiyun Huang ◽  
Ningsheng Liu ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cancer Cells ◽  
Cellular Proliferation ◽  
Human Gastric Cancer ◽  
Gastric Cancer Cells ◽  
Cox 2 ◽  
And Migration ◽  
Proliferation And Migration

Abstract Objective: The present study is designed to evaluate the anti-tumor effects of myrrh on human gastric cancer both in vitro and in vivo. Methods: The gastric cancer cell proliferation was determined by MTT assay. Apoptosis was measured by flow cytometry and Hoechst 33342 staining. Wound healing was performed to evaluate the effects of myrrh on the migration. COX-2, PCNA, Bcl-2, and Bax expressions were detected by Western blot analysis. A xenograft nude mice model of human gastric cancer was established to evaluate the anti-cancer effect of myrrh in vivo. Results: Myrrh significantly inhibited cellular proliferation, migration, and induced apoptosis in vitro as well as inhibited tumor growth in vivo. In addition, myrrh inhibited the expression of PCNA, COX-2, and Bcl-2 as well as increased Bax expression in gastric cancer cells. Conclusion: Myrrh may inhibit the proliferation and migration of gastric cancer cells, as well as induced their apoptosis by down-regulating the expression of COX-2.

Sign in / Sign up

Export Citation Format

Share Document