Soil Actinomycetes-derived Secondary Metabolites-Induced Apoptosis in Human Lung Cancer Cells

Rahil  Norbakhsh; Tohid Moradi  Gardeshi; Sina  Dalvand; Zahra Boroughani

doi:10.18502/ijml.v9i3.10908

Rahil Norbakhsh Department of Virology, Faculty of Medicine, Ahvaz Jundishapur University of Medical Sciences, Ahvaz, Iran
Tohid Moradi Gardeshi Department of Veterinary Sciences, Garmsar Branch, Islamic Azad University, Garmsar, Iran
Sina Dalvand International Campus, Shahid Sadoughi University of Medical Sciences, Yazd, Iran
Zahra Boroughani Department of Microbial Biotechnology, University of Tehran, Tehran, Iran

DOI: https://doi.org/10.18502/ijml.v9i3.10908

Keywords: Actinobacteria, Apoptosis, Doxorubicin, Lung neoplasms

Abstract

Background and Aims: Natural compounds derived from animal, plant, and microbial sources participate in treating various types of cancers, including lung cancer. This survey attempted to explore the anticancer activity of two novel metabolites extracted from soil-derived actinomycetes in the human lung cancer A549 cells.

Materials and Methods: The crude extracts of UTMC 638 and UTMC 877 secondary metabolites were obtained from the University of Tehran Microorganisms Collection (UTMC). When doxorubicin was applied as a positive control, cell viability, apoptosis detection, and mRNA expression were assessed by MTT assay, flow cytometry, and reverse transcription-quantitative polymerase chain reaction (RT-qPCR) technique.

Results: The results of the MTT assay showed that UTMC 638, UTMC 877, and doxorubicin reduce A549 cell viability in a concentration-dependent manner. Cell treatment with UTMC 877, UTMC 638, and doxorubicin could promote apoptosis in the A549 cell line. However, the effect of UTMC 638 on apoptotic induction was more than doxorubicin or UTMC 877. The q-RT-PCR results highlighted that the gene expression associated with apoptosis was augmented in the treated group compared to the untreated group.

Conclusion: Our findings provide evidence that the crude extract of UTMC 676 could promote apoptosis in A549 cells and can be a very promising source for designing a potent antitumor agent against lung cancer cells.