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pmid:29854840

Melittin Constrains the Expression of Identified Key Genes Associated with Bladder Cancer.

Zidan Jin · Jie Yao · Nianlin Xie · Libo Cai · Shuai Qi · Zhan Zhang · Bai Li

Journal of immunology research · 2018 doi:10.1155/2018/5038172

Paper

complete

Experiment

complete

Data

partial

Analysis

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Execution

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title
Melittin Constrains the Expression of Identified Key Genes Associated with Bladder Cancer.
doi
10.1155/2018/5038172
pmid
29854840
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Zidan Jin
[1]
Jie Yao
[2]
Nianlin Xie
[3]
Libo Cai
[4]
Shuai Qi
[5]
Zhan Zhang
[6]
Bai Li
journal
Journal of immunology research
year
2018
abstract
This work is aimed at investigating the effect of melittin on identified key genes in bladder cancer (BC) and further providing a theoretical basis for BC treatment. GSE35014 downloaded from the Gene Expression Omnibus (GEO) database was used to screen differentially expressed genes (DEGs) in BC cells and control. Results showed that a total of 389 upregulated and 169 downregulated genes were identified. Subsequently, GO analysis, KEGG pathway enrichment analysis, and PPI network analysis were employed to disclose the crucial genes and signaling pathways involved in BC. Fifteen module-related DEGs and their associated signaling pathways were obtained according to the PPI network and modular analyses. Based on the analysis of articles retrieved in the PubMed database, we found that melittin could induce apoptosis and constrain the progression of tumor cells as a result of regulating critical cancer-related signaling pathways, such as PI3K-Akt and TNF signaling pathways. Furthermore, PI3K-Akt and TNF signaling pathways were also found to be associated with module-related DEGs according to biological analyses. At last, qRT-PCR analysis demonstrated that melittin could constrain the expression of module-related DEGs (LPAR1, COL5A1, COL6A2, CXCL1, CXCL2, and CXCL3) associated with PI3K-Akt and TNF signaling pathways in BC cells. Functional assays revealed that melittin could constrain the proliferative and migrated abilities of BC cells. Conjointly, these findings provide a theoretical basis for these six genes as drug-sensitive markers of melittin in BC treatment.
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Limma package [30] was applied to identify DEGs between experimental and control groups with the cut-off criterion of P < 0.05 and absolute log2 FC > 1.
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Extracted from the GEO (https://www.ncbi.nlm.nih.gov/geo/) database, one microarray expression profile termed GSE35014 was therefore employed to identify DEGs associated with BC (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35014).
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sections[3] "2.1. Dataset Collection and Identification of DEGs in BC" paragraph 2
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Extracted from the GEO (https://www.ncbi.nlm.nih.gov/geo/) database, one microarray expression profile termed GSE35014 was therefore employed to identify DEGs associated with BC (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35014).
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sections[13] "3.1. Identification of DEGs in BC" paragraph 2
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According to microarray analysis, a total of 558 DEGs were achieved to be differentially expressed with a fold change > 2 between the BC cell group and control, as revealed in Figure 2. Among them, 389 upregulated and 169 downregulated genes were separately obtained as listed in Table 2.
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Extracted from the GEO (https://www.ncbi.nlm.nih.gov/geo/) database, one microarray expression profile termed GSE35014 was therefore employed to identify DEGs associated with BC (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35014).
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Extracted from the GEO (https://www.ncbi.nlm.nih.gov/geo/) database, one microarray expression profile termed GSE35014 was therefore employed to identify DEGs associated with BC (https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE35014).
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Complete file
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