Cytotoxicity of aptamer-conjugated chitosan encapsulated mycogenic gold nanoparticles in human lung cancer cells

The present work investigated the cytotoxicity of aptamer (Apt)-conjugated chitosan (CST) encapsulated mycogenic (Talaromyces purpureogenus (Tp)) gold nanoparticles (AuNPs) in human lung cancer cell line. A total of three steps were involved in the fabrication of Apt-CST-Tp-AuNPs: (i) mycogenic synthesis of Tp-AuNPs using mycelial extract of T. purpureogenus, (ii) encapsulation of the chitosan on Tp-AuNPs (CST-Tp-AuNPs), and (iii) conjugation of Apt in CST-Tp-AuNPs to form final material of Apt-CST-Tp-AuNPs. The nanoparticles Tp-AuNPs and Apt-CST-Tp-AuNPs were found to be hexagonal shaped with the size of 37.06 ± 6.70 nm and 62.05 ± 15.22 nm, respectively, observed by TEM analysis. But the DLS analysis showed the hydrodynamic size of Apt-CST-Tp-AuNPs was 91.67 ± 2.15 nm with a zeta potential of 47.31 ± 0.63 mV while Tp-AuNPs exhibited the hydrodynamic size of 56.13 ± 1.65 nm with a zeta potential of − 58.83 ± 1.64 mV. The size differences in the TEM and DLS analysis are attributed to the hydrodynamic nature of nanoparticles. The FTIR analysis demonstrated the capping of the mycelial extract on the surface of Tp-AuNPs and Apt-CST-Tp-AuNPs. The Apt-CST-Tp-AuNPs did not show cytotoxicity to human embryonic kidney cells (HEK293) while it showed ~ 60% of cell death in human lung cancer cells (A549). The annexin V FITC and PI staining results revealed that Apt-CST-Tp-AuNPs induced higher cell death (~ 8.60%) in A549 cells than Tp-AuNPs and CST-Tp-AuNPs. The Apt-CST-Tp-AuNPs triggered cytotoxicity in A549 cells through M1 phase cell cycle arrest and regulating the apoptosis-related protein (Bcl-2 and Bax) expressions. These results demonstrated the effective cytotoxic activity of Apt-CST-Tp-AuNPs in A549 cells.