scholarly journals ARHGAP42 promotes cell migration and invasion involving PI3K/Akt signaling pathway in nasopharyngeal carcinoma

2018 ◽  
Vol 7 (8) ◽  
pp. 3862-3874 ◽  
Author(s):  
Qian Hu ◽  
Xiao Lin ◽  
Linxiaoxiao Ding ◽  
Yinduo Zeng ◽  
Danmei Pang ◽  
...  
Keyword(s):  
Cell Migration ◽  
Nasopharyngeal Carcinoma ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Cell Migration And Invasion

scholarly journals NLRC5 promotes cell migration and invasion by activating the PI3K/AKT signaling pathway in endometrial cancer

2020 ◽  
Vol 48 (5) ◽  
pp. 030006052092535
Author(s):  
Yijun Fan ◽  
Zhen Dong ◽  
Yuchuan Shi ◽  
Shiying Sun ◽  
Bing Wei ◽  
...  
Keyword(s):  
Endometrial Cancer ◽  
Cell Migration ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Positive Role ◽  
Normal Endometrium ◽  
Cell Migration And Invasion

Objective NOD-like receptor family caspase recruitment domain family domain-containing 5 (NLRC5) is involved in the development of cancer. Our objective was to explore the role of NLRC5 in the progression of endometrial cancer (EC). Methods The roles of NLRC5 in migration and invasion of AN3CA EC cells were examined by cell wound-healing assay, Transwell migration, and invasion analysis. Overexpression of NLRC5 was achieved with NLRC5 plasmid, and knockdown of NLRC5 was achieved using small interfering (si)RNA-NLRC5 in AN3CA cells. The expression of NLRC5 was detected by immunohistochemical, western blot, and quantitative real-time PCR. LY294002 was used to inhibit the phosphatidylinositol 3-kinase (PI3K)/AKT signaling pathway. Results NLRC5 was downregulated in EC tissue compared with normal endometrium. Overexpression of NLRC5 led to upregulation of cell migration and invasion in AN3CA cells and expression of matrix metallopeptidase (MMP)-9. Inhibition of NLRC5 restricted migration and invasion of AN3CA cells and expression of MMP9. Overexpression of NLRC5 promoted the activation of PI3K/AKT signaling pathway. Inhibiting PI3K/AKT signaling pathway by using LY294002 blocked the positive role of NLRC5 in migration and invasion of AN3CA cells and expression of MMP9. Conclusions These results demonstrate that NLRC5 promotes EC progression by activating the PI3K/AKT signaling pathway.

MicroRNA-134 inhibits tumor stem cell migration and invasion in oral squamous cell carcinomas via downregulation of PI3K-Akt signaling pathway by inhibiting LAMC2 expression

2020 ◽  
Vol 29 (1) ◽  
pp. 51-67 ◽  
Author(s):  
Yong-Mei Zhou ◽  
Yi-Lin Yao ◽  
Wei Liu ◽  
Xue-Min Shen ◽  
Lin-Jun Shi ◽  
...  
Keyword(s):  
Stem Cells ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Signaling Pathway ◽  
Squamous Cell ◽  
Nude Mice ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Tumor Stem Cells ◽  
Akt Signaling Pathway

BACKGROUND: Oral squamous cell carcinoma (OSCC) is the most common malignant neoplasm of the mouth. Some studies have found that multiple microRNAs (miRs) participate in OSCC physiological and pathological processes. METHODS: We explored the mechanism of action of miR-134 in OSCC involving the PI3K-Akt signaling pathway. Different bioinformatics methods were used to analyze the potential genes and their related miRs in OSCC. Tumor stem cells were separated from OSCCs through magnetic cell sorting. Regulatory pattern between miR-134 and LAMC2 in OSCC was evaluated by ectopic expression, knockdown and reporter assay experiments. The expression of miR-134, LAMC2, genes in PI3K-Akt signaling pathway, and apoptosis-related genes was detected. Cell proliferation was assessed by MTT assay, cell invasion by scratch test, cell migration by Transwell assay, cell cycle and apoptosis by flow cytometry, and cell growth and migration by xenograft tumor in nude mice. LAMC2 was predicted as the crucial factor related to OSCC using different chip data, and miR-134 was predicted to specifically bind LAMC2 in all five databases. RESULTS: Overexpressed miR-134 or silenced LAMC2 was observed to inhibit cell proliferation, migration, invasion of OSCC cells, growth of subcutaneous xenograft in nude mice, as well as promote OSCC cell apoptosis. LAMC2, a target gene of miR-134, decreased following miR-134 promotion, while the PI3K-Akt signaling pathway was inactivated following LAMC2 knockdown. Furthermore, we also observed that the effect of overexpressed miR-134 was enhanced when LAMC2 was knocked down. CONCLUSIONS: Taken together, these findings suggest that miR-134-mediated direct downregulation of LAMC2 inhibits migration and invasion of tumor stem cells in OSCC by suppressing the PI3K-Akt signaling pathway.

scholarly journals The Overexpression of Acyl-CoA Medium-Chain Synthetase-3 (ACSM3) Suppresses the Ovarian Cancer Progression via the Inhibition of Integrin β1/AKT Signaling Pathway

2021 ◽  
Vol 11 ◽  
Author(s):  
Limei Yan ◽  
Zeping He ◽  
Wei Li ◽  
Ning Liu ◽  
Song Gao
Keyword(s):  
Ovarian Cancer ◽  
Cell Proliferation ◽  
Cell Migration ◽  
Signaling Pathway ◽  
Cancer Progression ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway ◽  
Integrin Β1

Ovarian cancer is considered as one of the most fatal gynecologic malignancies. This work aimed to explore the effects and regulatory mechanism of Acyl-CoA medium-chain synthetase-3 (ACSM3, a subunit of CoA ligases) in ovarian cancer progression. As well as employing CCK-8 assay, clone formation assay, and cell cycle analysis were carried out to investigate cell proliferation ability. Wound healing assay and transwell assay were subsequently used to assess cell migration and invasion. Mice xenografts were then conducted to measure the effects of ACSM3 on tumor development in vivo. Our bioinformatics analysis suggested that the expression of ACSM3 was down-regulated in ovarian cancer tissues, and the low expression level of ACSM3 might related with poorer overall survival than high mRNA expression of ACSM3 in ovarian cancer patients. We artificially regulated the expression of ACSM3 to evaluate its effects on ovarian cancer malignant phenotypes. Our data revealed that the overexpression of ACSM3 inhibited cell proliferation, migration, and invasion of ovarian cancer cells. In contrast, the knock-down of ACSM3 received the opposite results. Our western blot results showed that the Integrin β1/AKT signaling pathway was negatively regulated by ACSM3 expression. Moreover, ACSM3 overexpression-induced suppression of cell migration and invasion activities were abolished by the overexpression of ITG β1 (Integrin β1). Additionally, the growth of ovarian cancer xenograft tumors was also repressed by the overexpression of ACSM3. And ACSM3 interference obtained the contrary effects in vivo. In summary, ACSM3 acts as a tumor suppressor gene and may be a potential therapeutic target of ovarian cancer.

scholarly journals Ampelopsin Inhibits Cell Viability and Metastasis in Renal Cell Carcinoma by Negatively Regulating the PI3K/AKT Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-8
Author(s):  
Zhonghe Zhao ◽  
Yan Jiang ◽  
Zhongguo Liu ◽  
Qingyan Li ◽  
Tiantian Gao ◽  
...  
Keyword(s):  
Renal Cell Carcinoma ◽  
Cell Migration ◽  
Cell Viability ◽  
Cell Carcinoma ◽  
Signaling Pathway ◽  
Renal Cell ◽  
Inhibitory Effect ◽  
Akt Signaling ◽  
Migration And Invasion ◽  
Akt Signaling Pathway

Background. Previous studies have shown that Ampelopsin has an inhibitory effect on human tumors. However, the effect of Ampelopsin on renal cell carcinoma (RCC) is rarely reported. Therefore, this study aims to explain the role of Ampelopsin in RCC. Methods. Different concentrations of Ampelopsin (0, 10, 25, 50, and 100 μM) were used to treat 786-O cells. Cell viability was detected by MTT assay, colony formation assay, and flow cytometry assay. Transwell assay and Wound healing assay were used to detect cell migration and invasion. Western blot analysis was applied to detect protein expression. Results. Ampelopsin inhibited cell proliferation and induced apoptosis in RCC. And Ampelopsin can inhibit cell migration and invasion in RCC. All these results changed in a dose-dependent manner. Ampelopsin (100 uM) had the strongest inhibitory effect on cell viability and metastasis. In addition, Ampelopsin negatively regulated the PI3K/AKT signaling pathway in RCC cells. Moreover, Ampelopsin was only cytotoxic to RCC cells. Conclusion. Ampelopsin inhibits cell viability and metastasis in RCC by negatively regulating the PI3K/AKT signaling pathway.

scholarly journals M2 macrophage-derived exosomal microRNAs inhibit cell migration and invasion in gliomas through PI3K/AKT/mTOR signaling pathway

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Jie Yao ◽  
Zefen Wang ◽  
Yong Cheng ◽  
Chao Ma ◽  
Yahua Zhong ◽  
...  
Keyword(s):  
Cell Migration ◽  
Western Blot ◽  
Signaling Pathway ◽  
Target Gene ◽  
Glioma Cells ◽  
Mtor Signaling ◽  
Migration And Invasion ◽  
M2 Macrophage ◽  
Mtor Signaling Pathway ◽  
Cell Migration And Invasion

Abstract Background Glioma, the most common primary brain tumor, account Preparing figures for 30 to 40% of all intracranial tumors. Herein, we aimed to study the effects of M2 macrophage-derived exosomal microRNAs (miRNAs) on glioma cells. Methods First, we identified seven differentially expressed miRNAs in infiltrating macrophages and detected the expression of these seven miRNAs in M2 macrophages. We then selected hsa-miR-15a-5p (miR-15a) and hsa-miR-92a-3p (miR-92a) for follow-up studies, and confirmed that miR-15a and miR-92a were under-expressed in M2 macrophage exosomes. Subsequently, we demonstrated that M2 macrophage-derived exosomes promoted migration and invasion of glioma cells, while exosomal miR-15a and miR-92a had the opposite effects on glioma cells. Next, we performed the target gene prediction in four databases and conducted target gene validation by qRT-PCR, western blot and dual luciferase reporter gene assays. Results The results revealed that miR-15a and miR-92a were bound to CCND1 and RAP1B, respectively. Western blot assays demonstrated that interference with the expression of CCND1 or RAP1B reduced the phosphorylation level of AKT and mTOR, indicating that both CCND1 and RAP1B can activate the PI3K/AKT/mTOR signaling pathway. Conclusion Collectively, these findings indicate that M2 macrophage-derived exosomal miR-15a and miR-92a inhibit cell migration and invasion of glioma cells through PI3K/AKT/mTOR signaling pathway.

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