scholarly journals Identification of biomarkers associated with ovarian cancer based on transcriptome sequencing

2019 ◽  
Author(s):  
jiazhou chen ◽  
xiandong peng ◽  
min yu
Keyword(s):  
Ovarian Cancer ◽  
Cell Adhesion ◽  
Western Blot ◽  
Signaling Pathway ◽  
Transcriptome Sequencing ◽  
Akt Signaling ◽  
Serous Carcinoma ◽  
Receptor Interaction ◽  
List Type ◽  
Akt Signaling Pathway

AbstractObjectiveThis study aimed to explore more biomarkers associated with ovarian cancer.MethodsCell lines SKOV-3 (ovarian serous carcinoma cells) and MCV152 (benign ovarian epithelial tumor cell) were used in this study and performed transcriptome sequencing. The differentially expressed genes (DEGs) between ovarian cancer cells (SKOV-3) and controls (MCV152) were identified, followed by function enrichment analysis. The expression levels of genes involved in the key pathway were validated through PCR and western blot analyses.ResultsTotal 2,020 upregulated and 1,673 downregulated DEGs were obtained between SKOV3 and MCV152 cells. The upregulated and downregulated DEGs were significantly associated with cell adhesion. In addition, the upregulated DEGs were significantly involved in pathways of ECM-receptor interaction, and the downregulated DEGs were involved in PI3K-Akt signaling pathway. PCR and western blot analyses showed that genes (proteins) expression related to PI3K-Akt signaling pathway were in consistent with bioinformatics analysis.ConclusionCell adhesion and extracellular matrix (ECM)-receptor interaction may play an important role in the invasion of ovarian cancer. PI3K-Akt signaling pathway may be involved in the progression of ovarian cancer by up-regulating ANGPT2, FGF18, ITGB4 and ITGB8, and downregulating AKT3 and PIK3AP1.HighlightsCell adhesion and ECM-receptor interaction may play important roles in ovarian cancer invasion.PI3K-Akt signaling pathway may involve in ovarian cancer progression.ANGPT2, FGF18, ITGB4, ITGB8, AKT3 and PIK3AP1 may serve as biomarkers in ovarian cancer.

scholarly journals Overexpression of Long Noncoding RNA H19 Downregulates miR-140-5p and Activates PI3K/AKT Signaling Pathway to Promote Invasion, Migration and Epithelial-Mesenchymal Transition of Ovarian Cancer Cells

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Hao Xu ◽  
Yuan Ding ◽  
Xiangying Yang
Keyword(s):  
Ovarian Cancer ◽  
Western Blot ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Epithelial Mesenchymal Transition ◽  
Akt Signaling ◽  
Luciferase Reporter ◽  
Ovarian Cancer Cells ◽  
Akt Signaling Pathway ◽  
Mesenchymal Transition

Objective. The abnormal expression of LncRNA H19 and miR-140-5p has been linked to ovarian cancer (OC). Whether H19 directly regulates miR-140-5p in ovarian cancer cells has been unclear. In this study, we deeply explored the relationship between H19 and miR-140-5p in ovarian cancer and the mechanism of action in regulating OC progression. Methods. A total of 66 patients with OC admitted to the hospital from June 2017 to June 2019 were selected as the research group (RG), and meanwhile, 60 cases of healthy subjects were selected as the control group (CG). In addition, OC cells and normal ovarian epithelial cells were used to detect H19 and miR-140-5p expression levels and to analyze the effect of H19 on OC cells. The activation of the PI3K/AKT pathway and downstream proteins were analyzed by western blot. Results. H19 was highly expressed while miR-140-5p was lowly expressed in OC patients and cell lines ( P < 0.050 ). The proliferation, invasion, migration ability, and epithelial-mesenchymal transition (EMT) of OC cells were reduced after inhibiting H19 expression, and the apoptosis rate was increased. Transfection of cells with miR-140-5p mimics brought opposite effects. Online prediction and dual-luciferase reporter (DLR) confirmed that H19 directly binds miR-140-5p. Western blot assay indicated overexpression activated the PI3K/AKT signaling pathway in OC cells. Moreover, overexpression promoted tumor growth in nude mice and was suppressed by PI3K inhibitor. Conclusion. LncRNA H19 downregulation of miR-140-5p to activate the PI3K/AKT signaling pathway and promote the proliferation, invasion, migration and EMT of OC.

CNOT7 modulates biological functions of ovarian cancer cells via AKT signaling pathway

Life Sciences ◽  
2021 ◽  
Vol 268 ◽  
pp. 118996
Author(s):  
Jiangtao Yu ◽  
Xiaoli Hu ◽  
Xiuxiu Chen ◽  
Qiangyong Zhou ◽  
Qi Jiang ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Cancer Cells ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Ovarian Cancer Cells ◽  
Biological Functions ◽  
Akt Signaling Pathway

scholarly journals Gambogic acid protects LPS-induced apoptosis and inflammation in a cell model of neonatal pneumonia through the regulation of TrkA/Akt signaling pathway

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xu Gao ◽  
Jingya Dai ◽  
Guifang Li ◽  
Xinya Dai
Keyword(s):  
Western Blot ◽  
Signaling Pathway ◽  
Cell Model ◽  
Akt Signaling ◽  
Gambogic Acid ◽  
Akt Signaling Pathway ◽  
Western Blot Assay ◽  
A Cell ◽  
Induced Apoptosis ◽  
Apoptosis And Inflammation

Abstract Objective In this work, we investigated the effects of gambogic acid (GA) on lipopolysaccharide (LPS)-induced apoptosis and inflammation in a cell model of neonatal pneumonia. Method Human WI-38 cells were maintained in vitro and incubated with various concentrations of GA to examine WI-38 survival. GA-preincubated WI-38 cells were then treated with LPS to investigate the protective effects of GA on LPS-induced death, apoptosis and inflammation. Western blot assay was utilized to analyze the effect of GA on tropomyosin receptor kinase A (TrkA) signaling pathway in LPS-treated WI-38 cells. In addition, human AKT serine/threonine kinase 1 (Akt) gene was knocked down in WI-38 cells to further investigate the associated genetic mechanisms of GA in protecting LPS-induced inflammation and apoptosis. Results Pre-incubating WI-38 cells with low and medium concentrations GA protected LPS-induced cell death, apoptosis and inflammatory protein productions of IL-6 and MCP-1. Using western blot assay, it was demonstrated that GA promoted TrkA phosphorylation and Akt activation in LPS-treated WI-38 cells. Knocking down Akt gene in WI-38 cells showed that GA-associated protections against LPS-induced apoptosis and inflammation were significantly reduced. Conclusions GA protected LPS-induced apoptosis and inflammation, possibly through the activations of TrkA and Akt signaling pathway. This work may broaden our understanding on the molecular mechanisms of human neonatal pneumonia.

scholarly journals CEMIP promotes ovarian cancer development and progression via the PI3K/AKT signaling pathway

2019 ◽  
Vol 114 ◽  
pp. 108787 ◽  
Author(s):  
Fan Shen ◽  
Zhi-hong Zong ◽  
Yao Liu ◽  
Shuo Chen ◽  
Xiu-jie Sheng ◽  
...  
Keyword(s):  
Ovarian Cancer ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Cancer Development ◽  
Akt Signaling Pathway

scholarly journals Astragaloside positively regulated osteogenic differentiation of pre-osteoblast MC3T3-E1 through PI3K/Akt signaling pathway

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Wei Bing Jing ◽  
Hongjuan Ji ◽  
Rui Jiang ◽  
Jinlong Wang
Keyword(s):  
Western Blot ◽  
Osteogenic Differentiation ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Akt Signaling ◽  
Calcium Deposition ◽  
Control Group ◽  
Akt Signaling Pathway ◽  
Western Blot Assay

Abstract Background Osteoporosis is a widespread chronic disease characterized by low bone density. There is currently no gold standard treatment for osteoporosis. The aim of this study was to explore the role and mechanism of Astragaloside on osteogenic differentiation of MC3T3-E1 cells. Methods MC3T3-E1 cells were divided into control and different dose of Astragaloside (10, 20, 40, 50, and 60 μg/ml). Then, ALP and ARS staining were performed to identify the effects of Astragaloside for early and late osteogenic capacity of MC3T3-E1 cells, respectively. Real-time PCR and western blot were performed to assess the ALP, OCN, and OSX expression. PI3K/Akt signaling pathway molecules were then assessed by Western blot. Finally, PI3K inhibitor, LY294002, was implemented to assess the mechanism of Astragaloside in promoting osteogenic differentiation of MC3T3-E1 cells. Results Astragaloside significantly increased the cell viability than the control group. Moreover, Astragaloside enhanced the ALP activity and calcium deposition than the control groups. Compared with the control group, Astragaloside increased the ALP, OCN, and OSX expression in a dose-response manner. Western blot assay further confirmed the real-time PCR results. Astragaloside could significantly increase the p-PI3K and p-Akt expression than the control group. LY294002 partially reversed the promotion effects of Astragaloside on osteogenic differentiation of MC3T3-E1 cells. LY294002 partially reversed the promotion effects of Astragaloside on ALP, OCN, and OSX of MC3T3-E1 cells. Conclusion The present study suggested that Astragaloside promoted osteogenic differentiation of MC3T3-E1 cells through regulating PI3K/Akt signaling pathway.

scholarly journals Knockdown of JARID2 inhibits the proliferation and invasion of ovarian cancer through the PI3K/Akt signaling pathway

2017 ◽  
Vol 16 (3) ◽  
pp. 3600-3605 ◽  
Author(s):  
Jian Cao ◽  
Huiling Li ◽  
Guangquan Liu ◽  
Suping Han ◽  
Pengfei Xu
Keyword(s):  
Ovarian Cancer ◽  
Signaling Pathway ◽  
Akt Signaling ◽  
Akt Signaling Pathway ◽  
Proliferation And Invasion

miR-184 Inhibits Hypertrophic Scar Through Regulating Phosphatidylinositol 3-Kinase (PI3K)/Protein Kinase B (AKT) Signaling Pathway

2020 ◽  
Vol 10 (1) ◽  
pp. 133-138
Author(s):  
Peng Zhao ◽  
Junxia Qin ◽  
Lili Liang ◽  
Xinzhong Zhang
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Real Time ◽  
Signaling Pathway ◽  
Real Time Pcr ◽  
Hypertrophic Scar ◽  
Scar Tissue ◽  
Akt Signaling ◽  
Scar Formation ◽  
Akt Signaling Pathway

Hypertrophic scar (HS) is a process of tissue repair and healing, and excessive fibrosis of local tissue leads to scar formation. During HS formation, fibroblasts (Fb) proliferate, synthesize and secrete and promote HS development. miR-184 regulates skin formation and tissue development. However, miR-184’s role in HS remains unclear. miR-184 expression in HS patients and normal healthy (Control) tissues was measured by real-time PCR. pAKT expression was analyzed by Western blot. Fb cells from human HS were cultured and divided into 2 groups, siRNA NC group and miR-184 siRNA group followed by analysis of miR-184 expression by real time PCR, cell proliferation by MTT assay, secretion of inflammatory factors IL-1β and IL-6 by ELISA, as well as expression of pAKT and AKT by western blot. Compared with control group, miR-184 and pAKT expression was significantly increased in the HS group. Transfection of miR-184 siRNA into Fb significantly downregulated miR-184 expression, inhibited cell proliferation, promoted Caspase 3 activity, decreased IL-1β and IL-6 secretion, and reduced pAKT level (P < 0.05). miR-184 expression is increased in hypertrophic scar tissue. Down-regulation of miR-184 expression in proliferative scar tissue fibroblasts can down-regulate PI3K/AKT signaling pathway, inhibit inflammation, promote apoptosis, inhibit fibroblast proliferation, and regulate hypertrophic scar formation.

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