α-Conotoxin recombinant protein ImI-AFP3 efficiently inhibits the growth and migration of lung cancer cells
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Published on: June 26, 2019
Xiaobing Chen1, Zijuan Zou1, Wei Li1
1Hainan Provincial Key Laboratory of Carcinogenesis and Intervention, Hainan Medical University, Haikou, 571199, Hainan Province, PR China.
Abstract:
α-Conotoxin ImI is a selective antagonist of alpha7 nicotinic acetylcholine receptor (α7 nAChR) that is involved in cancer development. Human alpha fetoprotein domain 3 (AFP3) is a prototype of anticancer agents. In an effort to design drugs for anticancer treatments, we fused the ImI peptide to AFP3 as a fusion protein for testing. The fusion protein (ImI-AFP3) was highly expressed in the insect Bac-to-Bac system. The purified fusion protein was found to have improved anticancer activity and synergized with the drug gefitinib to inhibit the growth and migration of A549 and NCI-H1299 lung cancer cells. Our data have demonstrated that the recombinant protein ImI-AFP3 is a promising candidate for drug development to suppress lung cancer cell growth, especially to suppress hepatoid adenocarcinoma of the lung (HAL) cell growth.
Insights
Researchers fused α-conotoxin ImI with human alpha fetoprotein domain 3 (AFP3) to create a novel anticancer agent. This ImI-AFP3 fusion protein effectively inhibited lung cancer cell growth and migration, showing promise for new lung cancer therapies.
Area of Science:
- Biochemistry
- Molecular Biology
- Pharmacology
Background:
- Alpha7 nicotinic acetylcholine receptor (α7 nAChR) plays a role in cancer development.
- Alpha-conotoxin ImI is a selective α7 nAChR antagonist.
- Human alpha fetoprotein domain 3 (AFP3) is a known anticancer agent.
Purpose of the Study:
- To design and test a novel fusion protein, ImI-AFP3, for enhanced anticancer activity.
- To evaluate the efficacy of ImI-AFP3 in inhibiting lung cancer cell growth and migration.
- To assess the synergistic effect of ImI-AFP3 with gefitinib.
Main Methods:
- High-level expression of the ImI-AFP3 fusion protein using the insect Bac-to-Bac system.
- Purification of the recombinant ImI-AFP3 protein.
- In vitro testing of ImI-AFP3 on A549 and NCI-H1299 lung cancer cell lines, assessing growth and migration inhibition.
- Evaluation of synergy between ImI-AFP3 and gefitinib.
Main Results:
- The ImI-AFP3 fusion protein was successfully expressed and purified.
- ImI-AFP3 demonstrated improved anticancer activity against lung cancer cells.
- The fusion protein synergized with gefitinib to inhibit cancer cell growth and migration.
- Significant suppression of A549 and NCI-H1299 lung cancer cell proliferation and motility was observed.
Conclusions:
- The recombinant ImI-AFP3 protein is a promising candidate for lung cancer drug development.
- ImI-AFP3 shows potential for suppressing lung cancer cell growth, particularly hepatoid adenocarcinoma of the lung (HAL).
- Further investigation into ImI-AFP3 as a therapeutic agent for lung cancer is warranted.
