Insulin Receptor Substrate 1 Is Involved in the Phycocyanin-Mediated Antineoplastic Function of Non-Small Cell Lung Cancer Cells

• Published in: Molecules (Basel, Switzerland) Vol. 26; no. 16; p. 4711
• Main Authors: Hao, Shuai, Li, Qiancheng, Liu, Yuanpu, Li, Fannian, Yang, Qi, Wang, Jing, Wang, Chengtao
• Format: Journal Article
• Language: English
• Published: Basel MDPI AG 04.08.2021; MDPI
• Subjects: 1-Phosphatidylinositol 3-kinase; AKT protein; Algae; antineoplastic; Apoptosis; Cell growth; Cell proliferation; Colonies; Genes; Genotype & phenotype; Insulin; Insulin receptor substrate 1; insulin receptor substrate 1 (IRS-1); Liver cancer; Lung cancer; migration; non-small cell lung cancer (NSCLC); Non-small cell lung carcinoma; Phenotypes; Phosphorylation; Phycocyanin; proliferation; Proteins; siRNA; Substrates
• ISSN: 1420-3049; 1420-3049
• DOI: 10.3390/molecules26164711

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.