scholarly journals miR-520c and miR-373 upregulate MMP9 expression by targeting mTOR and SIRT1, and activate the Ras/Raf/MEK/Erk signaling pathway and NF-κB factor in human fibrosarcoma cells

2011 ◽  
Vol 227 (2) ◽  
pp. 867-876 ◽  
Author(s):  
Ping Liu ◽  
Michael J. Wilson
Keyword(s):  
Signaling Pathway ◽  
Erk Signaling ◽  
Mmp9 Expression ◽  
Fibrosarcoma Cells ◽  
Human Fibrosarcoma Cells

Telocytes Promote Hepatocellular Carcinoma by Activating The ERK Signaling Pathway and miR-942-3p/MMP9 Axis

2021 ◽  
Author(s):  
Ying Xu ◽  
Hu Tian ◽  
Chao Guang Luan ◽  
Kai Sun ◽  
Peng Jin Bao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Metastatic Cancer ◽  
Erk Signaling ◽  
Mmp9 Expression ◽  
Cancer Tissues

Abstract Background In China, hepatocellular carcinoma (HCC) is considered a malignant tumor with poor prognosis, frequent metastasis, and a high relapse rate. Telocytes participate in tumorigenic, invasive, and migratory processes by secreting functional proteins and transmitting cell-to-cell information, but theirs functions in HCC are still unknown. Methods TC counts and MMP9 expression in liver cancer tissues were measured using immunohistochemistry, western blotting, and RT-PCR. Primary TCs from liver para-cancer tissues were cultured in vitro. To verify the role of TCs in HCC, a metastatic cancer animal model was established using 3 types of liver cancer cell lines in vivo. Results TCs promoted HCC cell metastasis by MMP9 expression in vitro and in vivo. Platelet derived growth factor-alpha (PDGF-α), secreted by HCC cells, activated the Ras/ERK signaling pathway in TCs, thereby increasing MMP9 expression; however, this had no significant effect on TC proliferation and apoptosis. miR-942-3p suppressed MMP9 expression in TCs. Conclusion Our results reveal the role of TCs in HCC and the mechanisms by which they elicit their effects, and they may serve as novel prognostic markers for HCC.

scholarly journals Antioxidant Peptide Derived fromSpirulina maximaSuppresses HIF1α-Induced Invasive Migration of HT1080 Fibrosarcoma Cells

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Won Suk Kim ◽  
Won Kyo Jung ◽  
Sun Joo Park
Keyword(s):  
Cell Migration ◽  
Signaling Pathway ◽  
Ros Generation ◽  
Antioxidant Peptide ◽  
Intracellular Ros ◽  
Fibrosarcoma Cells ◽  
Ht1080 Cells ◽  
Human Fibrosarcoma Cells ◽  
Invasive Cell ◽  
Effective Cancer Therapy

Hypoxia causes the malignant progression of tumor cells; hence, it has been considered a central issue that must be addressed for effective cancer therapy. The initiation of tumor metastasis requires invasive cell migration. Here, we show that an antioxidant peptide derived fromSpirulina maximasuppresses hypoxia-induced invasive migration of HT1080 human fibrosarcoma cells. HT1080 cells treated with a hypoxia-inducing agent, CoCl2, exhibited an increase in invasive migration and intracellular reactive oxygen species (ROS), which is associated with an increase in the expression of hypoxia-induced factor 1α(HIF1α) accompanied by the activation of PI3K/Akt and ERK1/2. The inhibition of PI3K/Akt and ERK1/2 with specific inhibitors diminished the CoCl2-induced increase in HIF1αexpression and invasive cell migration. Moreover, CoCl2-induced HIF1αexpression was associated with an increase in the expression of molecules downstream ofβ-integrin, such as N-cadherin, vimentin, andβ-catenin. Therefore, theS. maximapeptide effectively attenuated the CoCl2-induced ROS generation and downregulated the HIF1αsignaling pathway involving PI3K/Akt, ERK1/2, andβ-integrin in cells. These results suggest that theS. maximaantioxidant peptide downregulates the HIF1αsignaling pathway necessary for hypoxia-induced invasive migration of HT1080 cells by attenuating intracellular ROS.S. maximapeptide may be an effective constituent in antitumor progression products.

scholarly journals Telocytes promote hepatocellular carcinoma by activating the ERK signaling pathway and miR-942-3p/MMP9 axis

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Ying Xu ◽  
Hu Tian ◽  
Chao Guang Luan ◽  
Kai Sun ◽  
Peng Jin Bao ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Liver Cancer ◽  
Signaling Pathway ◽  
Metastatic Cancer ◽  
Erk Signaling ◽  
Mmp9 Expression ◽  
Cancer Tissues

AbstractIn China, hepatocellular carcinoma (HCC) is considered a malignant tumor with poor prognosis, frequent metastasis, and a high relapse rate. Telocytes (TCs) participate in tumorigenic, invasive, and migratory processes by secreting functional proteins and transmitting cell-to-cell information, but their functions in HCC are still unknown. TC counts and MMP9 expression in liver cancer tissues were measured using immunohistochemistry, western blotting, and RT-PCR. Primary TCs from liver para-cancer tissues were cultured in vitro. To verify the role of TCs in HCC, a metastatic cancer animal model was established using three types of liver cancer cell lines in vivo. TCs promoted HCC cell metastasis by MMP9 expression in vitro and in vivo. Platelet-derived growth factor-alpha (PDGF-α), secreted by HCC cells, activated the Ras/ERK signaling pathway in TCs, thereby increasing MMP9 expression; Moreover, miR-942-3p suppressed MMP9 expression in TCs. Our results reveal the role of TCs in HCC and the mechanisms by which they elicit their effects, and they may serve as novel prognostic markers for HCC.

Sitagliptin relieves diabetic nephropathy fibrosis via the MAPK/ERK signaling pathway

2020 ◽  
Vol 45 (3) ◽  
Author(s):  
Shufeng Cheng ◽  
Liang Li ◽  
Chunquan Song ◽  
Huijing Jin ◽  
Shouguo Ma ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
Signaling Pathway ◽  
Erk Signaling

scholarly journals Exploration in the mechanism of fucosterol for the treatment of non-small cell lung cancer based on network pharmacology and molecular docking

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Xiaoling Li ◽  
Baixin Lin ◽  
Zhiping Lin ◽  
Yucui Ma ◽  
Qu Wang ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Molecular Docking ◽  
Small Cell Lung Cancer ◽  
Signaling Pathway ◽  
Cell Lung Cancer ◽  
Small Cell ◽  
Erk Signaling ◽  
Network Pharmacology ◽  
Protein Interaction Data ◽  
Small Cell Lung

AbstractFucosterol, a sterol isolated from brown algae, has been demonstrated to have anti-cancer properties. However, the effects and underlying molecular mechanism of fucosterol on non-small cell lung cancer remain to be elucidated. In this study, the corresponding targets of fucosterol were obtained from PharmMapper, and NSCLC related targets were gathered from the GeneCards database, and the candidate targets of fucosterol-treated NSCLC were predicted. The mechanism of fucosterol against NSCLC was identified in DAVID6.8 by enrichment analysis of GO and KEGG, and protein–protein interaction data were collected from STRING database. The hub gene GRB2 was further screened out and verified by molecular docking. Moreover, the relationship of GRB2 expression and immune infiltrates were analyzed by the TIMER database. The results of network pharmacology suggest that fucosterol acts against candidate targets, such as MAPK1, EGFR, GRB2, IGF2, MAPK8, and SRC, which regulate biological processes including negative regulation of the apoptotic process, peptidyl-tyrosine phosphorylation, positive regulation of cell proliferation. The Raf/MEK/ERK signaling pathway initiated by GRB2 showed to be significant in treating NSCLC. In conclusion, our study indicates that fucosterol may suppress NSCLC progression by targeting GRB2 activated the Raf/MEK/ERK signaling pathway, which laying a theoretical foundation for further research and providing scientific support for the development of new drugs.

Anti-angiogenesis Function of Ononin via Suppressing the MEK/Erk Signaling Pathway

2021 ◽  
Author(s):  
Guowei Gong ◽  
Yuzhong Zheng ◽  
Xiangpeng Kong ◽  
Zhen Wen
Keyword(s):  
Signaling Pathway ◽  
Erk Signaling
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