The Role of the miR-451-AMPK Signaling Pathway in Regulation of Cell Migration and Proliferation in Glioblastoma

The role of FGF21 plays in the development and progression of diabetic cardiomyopathy (DCM) has not been addressed. Here we demonstrated that type 1 diabetes decreased FGF21 levels in the blood, but up-regulated cardiac fgf21 expression about 40 fold at 2 months and 3-1.5 fold at 4 and 6 months after diabetes, which indicated a cardiac specific FGF21 adaptive up-regulation. To define the critical role of FGF21 in DCM, type 1 diabetes was induced in FGF21 knock out (FGF21KO) mice. At 1, 2 and 4 months after diabetes onset, no significant differences between FGF21KO and wild type (WT) diabetic mice in blood glucose and triglyceride levels were observed. But FGF21KO diabetic mice showed earlier and more severe cardiac dysfunction, remodeling and oxidative stress, as well as greater increase in cardiac lipid accumulation than WT diabetic mice. Mechanistically, FGF21 reduced palmitate-induced cardiac cell death, which was accompanied by up-regulation of cardiac Erk1/2, p38 MAPK and AMPK phosphorylation. Inhibition of each kinase with its inhibitor and/ or siRNA revealed that FGF21 prevents palmitate-induced cardiac cell death via up-regulating the Erk1/2-dependent p38 MAPK/AMPK signaling pathway. In vivo administration of FGF21, but not FGF21 plus ERK1/2 inhibitor, to diabetic mice significantly prevented cardiac cell death and reduced inactivation of Erk1/2, p38 MAPK and AMPK, and prevented cardiac remodeling and dysfunction at late-stage. Our results demonstrate that cardiac FGF21 decompensation may contribute to the development of DCM and FGF21 may be a therapeutic target for the treatment of diabetic cardiac damage via activation of Erk1/2-P38 MAPK-AMPK signaling.

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

Journal of International Medical Research ◽

10.1177/0300060520925352 ◽

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.

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EGCG inhibits Tat-induced LTR transactivation: Role of Nrf2, AKT, AMPK signaling pathway

Life Sciences ◽

10.1016/j.lfs.2012.03.013 ◽

2012 ◽

Vol 90 (19-20) ◽

pp. 747-754 ◽

Cited By ~ 16

Author(s):

Hong-Sheng Zhang ◽

Tong-Chao Wu ◽

Wei-Wei Sang ◽

Zheng Ruan

Keyword(s):

Signaling Pathway ◽

Ampk Signaling

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Role of the AMPK signaling pathway in early brain injury after subarachnoid hemorrhage in rats

Acta Neurochirurgica ◽

10.1007/s00701-015-2370-3 ◽

2015 ◽

Vol 157 (5) ◽

pp. 781-792 ◽

Cited By ~ 15

Author(s):

Ji-Yang An ◽

Li-Li Zhou ◽

Peng Sun ◽

Hong-Gang Pang ◽

Dan-Dong Li ◽

...

Keyword(s):

Subarachnoid Hemorrhage ◽

Brain Injury ◽

Signaling Pathway ◽

Early Brain Injury ◽

Ampk Signaling

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The Effects of Hispidulin on Bupivacaine-Induced Neurotoxicity: Role of AMPK Signaling Pathway

Cell Biochemistry and Biophysics ◽

10.1007/s12013-014-9888-5 ◽

2014 ◽

Vol 70 (1) ◽

pp. 241-249 ◽

Cited By ~ 18

Author(s):

Xinhuan Niu ◽

Jie Chen ◽

Ping Wang ◽

Hui Zhou ◽

Song Li ◽

...

Keyword(s):

Signaling Pathway ◽

Ampk Signaling

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The role of Src homology 2 containing protein tyrosine phosphatase 2 in vascular smooth muscle cell migration and proliferation

Acta Pharmacologica Sinica ◽

10.1038/aps.2010.168 ◽

2010 ◽

Vol 31 (10) ◽

pp. 1277-1283 ◽

Cited By ~ 10

Author(s):

Machender R Kandadi ◽

Matthew S Stratton ◽

Jun Ren

Keyword(s):

Smooth Muscle ◽

Cell Migration ◽

Smooth Muscle Cell ◽

Protein Tyrosine Phosphatase ◽

Tyrosine Phosphatase ◽

Src Homology 2 ◽

Smooth Muscle Cell Migration ◽

Src Homology ◽

Cell Migration And Proliferation

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Dexmedetomidine Inhibited Proliferation and Invasion of Cervical Cancer Cells by Inhibiting the Janus Tyrosine Kinase/Signal Transducer and Activator of Transcription Signaling Pathway

Journal of Biomaterials and Tissue Engineering ◽

10.1166/jbt.2021.2702 ◽

2021 ◽

Vol 11 (7) ◽

pp. 1293-1304

Author(s):

FenLan Xu ◽

Liying Xu ◽

Xiaoyan Xu ◽

Zhenhua Huang ◽

Liang Su

Keyword(s):

Cervical Cancer ◽

Cell Migration ◽

Western Blot ◽

Cell Viability ◽

Signaling Pathway ◽

Migration And Invasion ◽

Cell Migration And Invasion ◽

Stat Signaling ◽

Related Proteins

The role of anesthetics in the treatment of cancer has been reported, but the role of Dexmedetomidine (Dex) in the treatment of cervical cancer (CC) has not been reported.In this study, cell viability and proliferation were determined by MTT and cloning formation assay. The expression of proliferation-related proteins ki67 and PCNA was detected by western blot. Wound healing and transwell detected cell migration and invasion, and western blot detected the expression of migration and invasion related proteins MMP4 and MMP9, and epithelial-mesenchymal transformation (ETM)-related proteins N-cadherin, Snail, Vimentin and E-cadherin. Western blot also detected the expression of pathway related proteins p-JAK2, p-STAT1, p-STAT3, JAK2, STAT1 and STAT3. It showed that Dex inhibited the cell viability and proliferation of Hela and siHa and the expression of ki67 and PCNA were also inhibited. Dex inhibited the cell migration and invasion, and inhibited the expression of MMP4 and MMP9. In addition, Dex inhibited the expression of N-cadherin, Snail and Vimentin, and promoted the expression of E-cadherin. Dex inhibited the expression of p-JAK2, p-STAT1 and p-STAT3. After the addition of JAK/STAT signaling pathway agonist IL-6, the inhibition of Dex on proliferation, migration and invasion of CC cells was reversed. And the addition of JAK/STAT signaling pathway inhibitor AG490 could counteract the excitatory effect of IL-6 on the pathway, at which time the cell proliferation, invasion and migration were significantly increased. In conclusion, our study demonstrated that Dex inhibited proliferation, migration, and invasion of cells in CC by blocking the JAK/STAT signaling pathway.

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Role of MCPIP1 in the Endothelial-Mesenchymal Transition Induced by Silica

Cellular Physiology and Biochemistry ◽

10.1159/000452547 ◽

2016 ◽

Vol 40 (1-2) ◽

pp. 309-325 ◽

Cited By ~ 13

Author(s):

Jie Chao ◽

Xingang Wang ◽

Yuxia Zhang ◽

Tiebing Zhu ◽

Wei Zhang ◽

...

Keyword(s):

Cell Migration ◽

Umbilical Vein ◽

Mesenchymal Cell ◽

Akt Pathway ◽

Mesenchymal Transition ◽

Functional Changes ◽

Umbilical Vein Endothelial Cells ◽

Cell Migration And Proliferation ◽

Endothelial Mesenchymal Transition

Background: Silicosis is characterized by the accumulation of fibroblasts and the excessive deposition of extracellular matrix. Fibroblast generation via endothelial-mesenchymal transition (EndMT) is one process responsible for this accumulation of fibroblasts. However, the mechanisms underlying EndMT remain unknown. Methods: Human umbilical vein endothelial cells (HUVECs) were exposed to SiO2 (50 µg/cm2). Specific endothelial and mesenchymal markers were evaluated using immunofluorescence and western blot analysis. Functional changes were evaluated by analyzing cell migration and proliferation. LC3-adenovirus transfections were performed, and changes in autophagy were measured using a marker of autophagy. Results: SiO2 induced decreases in the endothelial cell-specific markers in HUVECs while dramatically increasing mesenchymal cell product levels and mesenchymal functions. Although MCPIP1 expression increased in parallel with the increase in specific mesenchymal cell products, the MCPIP1 expression level was not consistent with the observed decrease in specific endothelial marker expression. Autophagy mediated the effects of MCPIP1, as rapamycin and 3-MA enhanced and attenuated the effect of SiO2 on HUVECs, respectively. MAPKs and the PI3K/Akt pathway were involved in the regulation of MCPIP1 by SiO2, and Pyk2 and MLC-2 mediated cell migration. Conclusion: Our findings reveal a new potential function of MCPIP1, suggesting a possible mechanism of fibrosis in pulmonary silicosis.

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