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Analysis of Differential Expression Proteins of Paclitaxel-Treated Lung Adenocarcinoma Cell A549 Using Tandem Mass
1Academy of Chinese Medical Sciences, Henan University of Chinese Medicine, Zhengzhou, People's Republic of China.
Background:
Paclitaxel is widely used in the treatment of cancer and has a good effect in the treatment of non-small cell lung cancer. The combination of TMT proteomics and bioinformatics is used to systematically analyze the molecular mechanism of paclitaxel in the treatment of lung adenocarcinoma A549 cell, which is helpful to screen new therapeutic targets.
Methods:
MTT assay was used to analyze the inhibitory effect of paclitaxel on the proliferation of A549 cells. The proteins were identified by TMT quantitative proteomics and the differential expression proteins (DEPs) database was constructed. The DEPs were enriched by Gene Ontology (GO) and KEGG pathway annotation. Based on the information in the STRING database, find the interaction between DEPs, and the protein-protein interaction (PPI) networks of DEPs were constructed and analyzed by using the Cytoscape software. According to the PPI network results, select the hub proteins from DEPs for WB verification.
Results:
A total of 5449 proteins were identified in A549 by TMT proteomics. Compared with the control group, 281 DEPs were significantly up-regulated and 218 were significantly down-regulated after paclitaxel treatment. GO functional analysis, we found that the main functions of these DEPs are binding, catalytic activity, molecular function regulator and so on. They are mainly involved in cellular process, metabolic process, biological regulation and so on. KEGG analysis showed that the three most significant signal transduction pathways of DEPs enrichment were DNA replication, steroid biosynthesis, oxidative phosphorylation. In PPI network, there are 294 nodes among which CDK1, MCM2-5 and PCNA are located at the center of proteins interaction. WB analysis confirmed that the expression of CDK1 was significantly down-regulated, consistent with the TMT results.
Conclusion:
Paclitaxel significantly increased the expression of tubulin, binding tubulin to promote A549 cell death. In addition, paclitaxel significantly inhibited the expression of hub proteins, DNA replication and cell cycle pathways, thus killing lung adenocarcinoma cell A549. These findings will enhance the understanding of the mechanism of paclitaxel in the treatment of lung adenocarcinoma cell A549 and provide new valuable targets.
Insights
Paclitaxel treatment of lung adenocarcinoma A549 cells revealed key molecular changes. This study identified novel therapeutic targets by analyzing protein expression and interactions, enhancing our understanding of paclitaxel
Area of Science:
- Proteomics and Bioinformatics
- Molecular Oncology
- Cancer Therapeutics
Background:
- Paclitaxel is a crucial chemotherapy agent for non-small cell lung cancer.
- Understanding the molecular mechanisms of paclitaxel in lung adenocarcinoma is vital for identifying new therapeutic strategies.
- This study investigates paclitaxel's effects on A549 lung adenocarcinoma cells using TMT proteomics and bioinformatics.
Purpose of the Study:
- To systematically analyze the molecular mechanism of paclitaxel in A549 lung adenocarcinoma cells.
- To identify differentially expressed proteins (DEPs) and their associated pathways.
- To screen for potential new therapeutic targets for lung adenocarcinoma treatment.
Main Methods:
- TMT quantitative proteomics was employed to identify proteins in A549 cells treated with paclitaxel.
- Bioinformatic analyses, including Gene Ontology (GO) and KEGG pathway enrichment, were performed on DEPs.
- Protein-protein interaction (PPI) networks were constructed using STRING and visualized with Cytoscape to identify hub proteins, followed by Western blot (WB) verification.
Main Results:
- A total of 5449 proteins were identified, with 281 upregulated and 218 downregulated DEPs after paclitaxel treatment.
- GO analysis indicated DEPs are involved in binding, catalytic activity, and cellular and metabolic processes.
- KEGG pathway analysis highlighted DNA replication, steroid biosynthesis, and oxidative phosphorylation as significantly affected pathways. CDK1, MCM2-5, and PCNA were identified as central hub proteins in the PPI network, with WB confirming CDK1 downregulation.
Conclusions:
- Paclitaxel promotes A549 cell death by increasing tubulin expression and binding.
- Paclitaxel inhibits key proteins, DNA replication, and cell cycle pathways, leading to lung adenocarcinoma cell death.
- These findings provide a deeper understanding of paclitaxel's mechanism in lung adenocarcinoma and suggest novel therapeutic targets.
