scholarly journals Effect of T‑cadherin on the AKT/mTOR signaling pathway, gastric cancer cell cycle, migration and invasion, and its association with patient survival rate

2019 ◽  
Author(s):  
Jianqing Lin ◽  
Zhiyao Chen ◽  
Zhijun Huang ◽  
Feng Chen ◽  
Zeyi Ye ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cell Cycle ◽  
Survival Rate ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Patient Survival ◽  
Migration And Invasion ◽  
Mtor Signaling Pathway ◽  
Patient Survival Rate

TULP3 Silencing Suppresses Cell Proliferation, Migration and Invasion in Gastric Cancer Via the PTEN/Akt/Snail Signaling Pathway

2021 ◽  
Author(s):  
Rui Liu ◽  
Jun Song ◽  
Qingsheng Fu ◽  
Gang Liu ◽  
Chengxiong Zhang ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Western Blotting ◽  
Molecular Mechanisms ◽  
Gastric Cancer Cell ◽  
Gene Knockout ◽  
Migration And Invasion ◽  
Quantitative Detection ◽  
Mouse Xenograft Model

Abstract Purpose Tubby-like protein 3 (TULP3), a member of the tubby family, has been related to the development of nervous system by gene knockout researches. Nevertheless, the regulatory mechanism and role of TULP3 in the gastric cancer are not clear. Current research is the first probe into the regulatory effect of TULP3 in the gastric cancer. Methods Western blotting together with real time polymerase chain reaction (PCR) were employed for the quantitative detection of TULP3 expression in the gastric cancer and consecutive non-cancerous tissues, and gastric cancer cells. Kaplan-Meier method along with Log-rank test was exploited for the determination of the disease-free survival rate and overall survival time of patient containing with different expression of TULP3 in tumors. The roles of TULP3 in invasion, migration as well as proliferation of the gastric cancer cell in vivo and in vitro through utilizing colony formation test, MTT test, wound-healing test, transwell test and mouse xenograft model. Western blotting assay was implemented in order to clarify the potential molecular mechanisms. Furthermore, electron microscopy and western blot were evaluated TULP3 expression in gastric cancer patient extracted serum exosomes. Results TULP3 expression levels were remarkably up-regulated in the gastric cancer tissues and cells. Subsequent functional assays demonstrated that TULP3 downregulation suppressed invasion, migration as well as the proliferation of the gastric cancer cell. Mechanism assays depicted that the PTEN/Akt/Snail signaling pathway can inhibit invasion, migration as well as the proliferation of the gastric cancer cell via TULP3 silencing. Finally, we found that the expression of TULP3 could be determined in the extracted serum exons. The expression of TULP3 in gastric cancer group was higher in comparison with normal group. Conclusion Our outcomes reveal that TULP3 probably play a role in the diagnosis together with the prognostic biomarkers of gastric cancer.

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

2018 ◽  
Vol 19 (10) ◽  
pp. 2986 ◽  
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.

NUCKS1 promotes gastric cancer cell aggressiveness by upregulating IGF-1R and subsequently activating the PI3K/Akt/mTOR signaling pathway

2018 ◽  
Vol 40 (2) ◽  
pp. 370-379 ◽  
Author(s):  
Ya-kai Huang ◽  
Wei-ming Kang ◽  
Zhi-qiang Ma ◽  
Yu-qin Liu ◽  
Li Zhou ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Mtor Signaling ◽  
Mtor Signaling Pathway

scholarly journals MiR-450a-5p Inhibits Gastric Cancer Cell Proliferation, Migration, and Invasion and Promotes Apoptosis via Targeting CREB1 and Inhibiting AKT/GSK-3β Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Ya-Jun Zhao ◽  
Jun Zhang ◽  
Yong-Cang Wang ◽  
Liang Wang ◽  
Xin-Yang He
Keyword(s):  
Gastric Cancer ◽  
Cell Proliferation ◽  
Signaling Pathway ◽  
Cancer Cell ◽  
Gastric Cancer Cell ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Gastric Cancer Cell Proliferation ◽  
Gsk 3Β

Gastric cancer seriously affects human health and research on gastric cancer is attracting more and more attentions. In recent years, molecular targets have become the research focus. Accumulating evidence indicates that miR-450a-5p plays a critical role in cancer progression. However, the biological role of miR-450a-5p in gastric carcinogenesis remains largely unknown. In this study, we explore the effects and mechanisms of miR-450a-5p on the development and progression of gastric cancer. We used gain-of-function approaches to investigate the role of miR-450a-5p on gastric cancer cell proliferation, migration, invasion, and apoptosis using biological and molecular techniques including real-time quantitative PCR (RT-qPCR), CCK-8, colony formation, flow cytometry, Western blot, wound healing, transwell chamber, dual luciferase reporter, and tumor xenograft mouse model. We found that gastric cancer cells have low expression of miR-450a-5p and overexpression of miR-450a-5p inhibited gastric cancer cell proliferation, migration and invasion, and induced apoptosis in vitro. Moreover, we demonstrated that ectopic expression of miR-450a-5p inhibited gastric cancer growth in vivo. At the molecular level, overexpression of miR-450a-5p significantly increased the expression of pro-apoptotic proteins, including caspase-3, caspase-9, and Bax, and inhibited the expression of anti-apoptotic protein Bcl-2. Luciferase reporter experiment suggested that camp response element binding protein 1 (CREB1) had a negative correlation with miR-450a-5p expression, and knockdown of CREB1 alleviated gastric cancer growth. Furthermore, we also found that miR-450a-5p inhibited the activation of AKT/GSK-3β signaling pathway to inhibit the progression of gastric cancer. Collectively, miR-450a-5p repressed gastric cancer cell proliferation, migration and invasion and induced apoptosis through targeting CREB1 by inhibiting AKT/GSK-3β signaling pathway. MiR-450a-5p could be a novel molecular target for the treatment of gastric cancer.

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