1. Insulin Receptor Substrate 1 Is Involved in the Phycocyanin-Mediated Antineoplastic Function of Non-Small Cell Lung Cancer Cells.
- Author
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Hao S, Li Q, Liu Y, Li F, Yang Q, Wang J, and Wang C
- Subjects
- Apoptosis drug effects, Carcinoma, Non-Small-Cell Lung genetics, Cell Line, Tumor, Cell Movement drug effects, Cell Proliferation drug effects, Down-Regulation drug effects, Gene Expression Regulation, Neoplastic drug effects, Gene Knockdown Techniques, Humans, Lung Neoplasms genetics, Proto-Oncogene Proteins c-akt metabolism, Antineoplastic Agents pharmacology, Carcinoma, Non-Small-Cell Lung metabolism, Carcinoma, Non-Small-Cell Lung pathology, Insulin Receptor Substrate Proteins metabolism, Lung Neoplasms metabolism, Lung Neoplasms pathology, Phycocyanin pharmacology
- Abstract
Phycocyanin, derived from marine algae, is known to have noteworthy antineoplastic properties. However, the underlying mechanism involved in phycocyanin-mediated anti-growth function on non-small cell lung cancer (NSCLC) cells is still ambiguous. Here, we investigated the mechanism of action of phycocyanin on H1299, A549, and LTEP-a2 cells. According to the results obtained, insulin receptor substrate 1 (IRS-1) expression was reduced by phycocyanin. Cell phenotype tests showed that siRNA knockdown of IRS-1 expression significantly inhibited the growth, migration, colony formation, but promoted the apoptosis of NSCLC cells. Meanwhile, phycocyanin and IRS-1 siRNA treatment both reduced the PI3K-AKT activities in NSCLC cells. Moreover, overexpression of IRS-1 accelerated the proliferation, colony formation, and migration rate of H1299, A549, and LTEP-a2 cells, which was contradicting to the knockdown results. Overall, this study uncovered a regulatory mechanism by which phycocyanin inhibited the growth of NSCLC cells via IRS-1/AKT pathway, laying the foundation for the potential target treatment of NSCLC.
- Published
- 2021
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