Promising Anticancer Effect of Aurisin A Against the Human Lung Cancer A549 Cell Line

Abstract

Objective: To investigate the anticancer effect of aurisin A and the underlying mechanisms of its action on the human lung cancer A549 cell line. Methods: Cell viability was determined by sulforhodamine B (SRB) assay, while cell cycle distribution and apoptosis were measured by flow cytometry. The molecular underlying mechanisms of anti-cancer properties of aurisin A was determined by western blot analysis. Results: Aurisin A exerts its anticancer effects by inhibiting cell growth (p<0.001), increasing the proportion of cells at the G0/G1 phase (p<0.001), and decreasing the expression of cyclin D (p<0.05) and cyclin-dependent kinase 4 (Cdk-4) (p<0.001). Nuclear morphological changes were observed in aurisin A-treated cells, demonstrated by a dose-dependent increase in the number of apoptosis cells (p<0.001). After aurisin A treatment, B-cell lymphoma 2 (Bcl-2) was down-regulated (p<0.05), cleaved caspase-3 was up-regulated (p<0.05). In addition, aurisin A inhibits migration of cancer cells in a dose-dependent manner (p<0.001) and decreases the expression of epidermal growth factor receptor (EGFR) (p<0.05) and phosphorylated p38 (pp38) (p<0.05). Conclusion: These results indicated that in-vitro treatment of aurisin A against this human lung cancer cell line inhibits cell proliferation and migration, and induces apoptosis and cell-cycle arrest. Aurisin A is a promising anticancer agent for use against human lung cancer.

<p>miR-519d-3p Overexpression Inhibits P38 and PI3K/AKT Pathway via Targeting VEGFA to Attenuate the Malignant Biological Behavior of Non-Small Cell Lung Cancer</p>

“…p38MARK is also involved in the regulation of NSCLC. Boueroy et al 34 found that aurisin A could inhibit migration of cancer cells and decrease the expression of epidermal growth factor receptor (EGFR) and phosphorylated p38 (pp38). Xu etal 35 reported that TGFβRII knockdown can inhibit cell proliferation, invasion, and induce apoptosis by inhibiting PI3K/Akt and p38 MAPK pathway, and inhibit MMPs and VEGF expression in A549 cells.…”

Activity of aurisin A isolated from Neonothopanus nambi against methicillin-resistant Staphylococcus aureus strains

“…R.H. Petersen & Krisai and deposited at DSMZ Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH under the accession number DSM 24013. Previous researchers have shown that N. nambi produced many different bioactive secondary metabolites exhibiting nematicidal activity against root-knot nematode Meloidogyne incognita ( Bua-art et al, 2011 ), cytotoxicity against cancer cells ( Kanokmedhakul et al, 2012 , Boueroy et al, 2020 , Boueroy et al, 2021 , Wisetsai et al, 2021 ), and antimalarial, antimycobacterial ( Kanokmedhakul et al, 2012 ) and antibacterial ( Sangsopha et al, 2020 , Wisetsai et al, 2021 ) activities. In this study, a bioactive compound was isolated from N. nambi DSM 24013 and evaluated for the first time for inhibitory effects against different reference and clinical MRSA strains, as well as presence of synergistic effects when combined with other antistaphylococcal antibiotics before proceeding to understand its mechanism/s of action in future studies.…”

Aurisin A Complexed with 2,6-Di-O-methyl-β-cyclodextrin Enhances Aqueous Solubility, Thermal Stability, and Antiproliferative Activity against Lung Cancer Cells

“…This compound exhibits various biological and pharmacological activities, including antimycobacterial activity toward Mycobacterium tuberculosis , antimalarial property against Plasmodium falciparum [ 1 ], and anticancer potential toward lung cancer cells (NCI-H187 and A549) [ 1 , 2 ], breast cancer cells (BC1), epidermoid carcinoma cells (KB), cholangiocarcinoma cells (KKU-100, KKU-139, KKU-156, KKU-213, and KKU-214) [ 1 ], and cervical cancer cells (Hela, CaSki, and SiHa), with no cytotoxic effect on normal white blood cells [ 3 ]. AA exerts its anticancer effects by (i) inhibiting cancer cell growth and migration and (ii) inducing cell cycle arrest and apoptosis through activating caspase-3/9 as well as decreasing the expression of cyclin D1, cyclin-dependent kinase 2/4 (Cdk-2/4), B-cell lymphoma 2 (Bcl-2), epidermal growth factor receptor (EGFR), phosphorylated p38 (pp38), and vascular endothelial growth factor (VEGF) [ 2 , 3 ]. Although AA possesses promising biological and pharmacological activities, its low water solubility limits its use for further applications as herbal medicines or healthcare products.…”