scholarly journals iTRAQ-Based Proteomic Analysis of Ginsenoside F2on Human Gastric Carcinoma Cells SGC7901

2016 ◽  
Vol 2016 ◽  
pp. 1-21 ◽  
Author(s):  
Qian Mao ◽  
Pin-Hu Zhang ◽  
Jie Yang ◽  
Jin-Di Xu ◽  
Ming Kong ◽  
...  

Ginsenoside F2(F2), a protopanaxdiol type of saponin, was reported to inhibit human gastric cancer cells SGC7901. To better understand the molecular mechanisms of F2, an iTRAQ-based proteomics approach was applied to define protein expression profiles in SGC7901 cells in response to lower dose (20 μM) and shorter duration (12 hour) of F2treatment, compared with previous study. 205 proteins were screened in terms of the change in their expression level which met our predefined criteria. Further bioinformatics and experiments demonstrated that F2treatment downregulated PRR5 and RPS15 and upregulated RPL26, which are implicated in ribosomal protein-p53 signaling pathway. F2also inhibited CISD2, Bcl-xl, and NLRX1, which are associated with autophagic pathway. Furthermore, it was demonstrated that F2treatment increased Atg5, Atg7, Atg10, and PUMA, the critical downstream effectors of ribosomal protein-p53 signaling pathway, and Beclin-1, UVRAG, and AMBRA-1, the important molecules in Bcl-xl/Beclin-1 pathway. The 6 differentially abundant proteins, PRR5, CISD2, Bcl-xl, NLRX1, RPS15, and RPL26, were confirmed by western blot. Taken together, ribosomal protein-p53 signaling pathway and Bcl-xl/Beclin-1 pathway might be the most significantly regulated biological process by F2treatment in SGC7901 cells, which provided valuable insights into the deep understanding of the molecular mechanisms of F2for gastric cancer treatment.

2019 ◽  
Author(s):  
Jarmila Nahálková

The protein-protein interaction network of seven pleiotropic proteins (PIN7) contains proteins with multiple functions in the aging and age-related diseases (TPPII, CDK2, MYBBP1A, p53, SIRT6, SIRT7, and BSG). At the present work, the pathway enrichment, the gene function prediction and the protein node prioritization analysis were applied for the examination of main molecular mechanisms driving PIN7 and the extended network. Seven proteins of PIN7 were used as an input for the analysis by GeneMania, a Cytoscape application, which constructs the protein interaction network. The software also extends it using the interactions retrieved from databases of experimental and predicted protein-protein and genetic interactions. The analysis identified the p53 signaling pathway as the most dominant mediator of PIN7. The extended PIN7 was also analyzed by Cytohubba application, which showed that the top-ranked protein nodes belong to the group of histone acetyltransferases and histone deacetylases. These enzymes are involved in the reverse epigenetic regulation mechanisms linked to the regulation of PTK2, NFκB, and p53 signaling interaction subnetworks of the extended PIN7. The analysis emphasized the role of PTK2 signaling, which functions upstream of the p53 signaling pathway and its interaction network includes all members of the sirtuin family. Further, the analysis suggested the involvement of molecular mechanisms related to metastatic cancer (prostate cancer, small cell lung cancer), hemostasis, the regulation of the thyroid hormones and the cell cycle G1/S checkpoint. The additional data-mining analysis showed that the small protein interaction network MYBBP1A-p53-TPPII-SIRT6-CD147 controls Warburg effect and MYBBP1A-p53-TPPII-SIRT7-BSG influences mTOR signaling and autophagy. Further investigations of the detail mechanisms of these interaction networks would be beneficial for the development of novel treatments for aging and age-related diseases.


2019 ◽  
Vol 30 ◽  
pp. vii11
Author(s):  
S. Gurzu ◽  
H. Sugimura ◽  
R.I. Van Staden ◽  
H. Yamada ◽  
I. Jung

Dose-Response ◽  
2020 ◽  
Vol 18 (1) ◽  
pp. 155932582091418
Author(s):  
Guangyao He ◽  
Anzhou Tang ◽  
Mao Xie ◽  
Wei Xia ◽  
Pengcheng Zhao ◽  
...  

Radiotherapy is an effective treatment for local solid tumors, but the mechanism of damage to human body caused by radiation therapy needs further study. In this study, gene expression profiles of human peripheral blood samples exposed to different doses and rates of ionizing radiation (IR) were used for bioinformatics analysis to investigate the mechanism of IR damage and radiation-induced bystander effect (RIBE). Differentially expressed genes analysis, weighted gene correlation network analysis, functional enrichment analysis, hypergeometric test, gene set enrichment analysis, and gene set variation analysis were applied to analyze the data. Moreover, receiver operating characteristic curve analysis was performed to identify core genes of IR damage. Weighted gene correlation network analysis identified 3 modules associated with IR damage, 2 were positively correlated and 1 was negatively correlated. The analysis showed that the positively correlated modules were significantly involved in apoptosis and p53 signaling pathway, and ESR1, ATM, and MYC were potential transcription factors regulating these modules. Thus, the study suggested that apoptosis and p53 signaling pathway may be the potential molecular mechanisms of IR damage and RIBE, which could be driven by ESR1, ATM, and MYC.


2021 ◽  
Author(s):  
Kento Kurashima ◽  
Atsushi Shiozaki ◽  
Michihiro Kudou ◽  
Hiroki Shimizu ◽  
Tomohiro Arita ◽  
...  

2021 ◽  
Author(s):  
Fengshou Chen ◽  
Haijia Hou ◽  
Jie Han ◽  
Bing Tang

Abstract Background Accumulating evidence suggests the existence sex associated differences in the Chronic Obstructive Pulmonary Disease (COPD). However, limited knowledge exists on the molecular mechanisms underlying sex associated differences in COPD patients. Methods The GSE8581 dataset obtained from the GEO database was used to analyze differentially expressed genes (DEGs). Then enrichment analysis for DEGs were conducted through Metascape. PPI and the hub genes-pathway networks were constructed using the STRING database and Cytoscape software. Finally, the CTD was used to examine the relationships between the hub DEGs and COPD. Results The results revealed that different subsets of DEGs had different characteristics in GO functions and KEGG pathways. Different subsets of hub genes were obtained based on PPI network. The study then constructed the hub genes-pathway network for different subsets to explore the key signaling pathways and hub genes involved. The findings showed that NRAS and RAC1 functioned through “Rap1 signaling pathway” and “PI3K-Akt signaling pathway”, in male COPD patients. On the other hand, “Cholesterol metabolism” was among the important pathways in female COPD patients while the hub genes, APOE and APOC3 functioned through “Cholesterol metabolism”. Moreover, “Ubiquitin mediated proteolysis” and the “p53 signaling pathway” were shown to play more important roles in male COPD patients compared to their female counterparts. Furthermore, CDK2 and UBE2N were the hub genes involved in “p53 signaling pathway” and “Ubiquitin mediated proteolysis”, respectively. Finally the study identified the relationship between the hub genes and COPD in CTD. Conclusions The present study uncovered different molecular mechanisms in COPD patients based on sex. Additionally, distinct pathways and hub genes including NRAS, RAC1, APOE, APOC3, CDK2 and UBE2N were identified in the two genders of COPD patients. Further studies are needed to explore individualized treatment for COPD based on the findings.


2021 ◽  
Vol 17 (12) ◽  
pp. 3145-3157
Author(s):  
Jingjing Hou ◽  
Lin Wang ◽  
Jiabao Zhao ◽  
Huiqin Zhuo ◽  
Jia Cheng ◽  
...  

2018 ◽  
Vol 2018 ◽  
pp. 1-16 ◽  
Author(s):  
Shui Liu ◽  
Xiaoxiao Yao ◽  
Dan Zhang ◽  
Jiyao Sheng ◽  
Xin Wen ◽  
...  

Hepatocellular carcinoma (HCC) accounts for a significant proportion of liver cancer, which has become the second most common cause of cancer-related mortality worldwide. To investigate the potential mechanisms of invasion and progression of HCC, bioinformatics analysis and validation by qRT-PCR were performed. We found 237 differentially expressed genes (DEGs) including EGR1, FOS, and FOSB, which were three cancer-related transcription factors. Subsequently, we constructed TF-gene network and miRNA-TF-mRNA network based on data obtained from mRNA and miRNA expression profiles for analysis of HCC. We found that 42 key genes from the TF-gene network including EGR1, FOS, and FOSB were most enriched in the p53 signaling pathway. The qRT-PCR data confirmed that mRNA levels of EGR1, FOS, and FOSB all were decreased in HCC tissues. In addition, we confirmed that the mRNA levels of CCNB1, CCNB2, and CHEK1, three key markers of the p53 signaling pathway, were all increased in HCC tissues by bioinformatics analysis and qRT-PCR validation. Therefore, we speculated that miR-181a-5p, which was upregulated in HCC tissues, could regulate FOS and EGR1 to promote the invasion and progression of HCC by p53 signaling pathway. Overall, the study provides support for the possible mechanisms of progression in HCC.


2015 ◽  
Vol 47 (5) ◽  
pp. 1725-1734 ◽  
Author(s):  
JUNYU HE ◽  
GUANGCHAO ZHU ◽  
LU GAO ◽  
PAN CHEN ◽  
YUEHUA LONG ◽  
...  

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