Background: Apoptosis induction is one of the effective mechanisms in cancer therapy. So far, various natural sources have been identified for inducing apoptosis in cancer cells. This study proposed identifying promising active drug pharmacophores of soil actinomycetes with the capability of apoptosis induction in A549 cells, a human alveolar adenocarcinoma cell line. Methods: The crude extract of Nocardia carnea UTMC 863 was obtained from UTBC (University of Tehran Biocompound Collection). After 48 hours of exposure, cell viability, gene expression, and apoptosis rate were determined using MTT, quantitative real-time-PCR, and flow cytometry. Results: The MTT assay exhibited that the effective concentrations of UTMC863 and doxorubicin (positive control) were 24 µg/ml and 1 µM, respectively. UTMC 863 with a 24 µg/ml concentration and doxorubicin could induce apoptosis in the A549 cell line. Also, apoptosis-related gene expression increased in the UTMC863 group compared to the untreated group (p<0.01). Conclusions: The crude extract of Nocardia carnea UTMC 863 can induce apoptosis in A549 cells, and it may be one of the promising pharmacophores for cancer therapy.
Background & Aims: Bacterial metabolites are extremely rich resources for discovering new compounds with different biological activities. Metabolites of actinomycetes have significant potential for the production of anticancer compounds. The purpose of this research is to investigate the effects of two secondary metabolites of soil actinomycetes, UTMC 676 and UTMC 919, on apoptosis induction and their related genes in the human non-small cell lung carcinoma cell line, A549. Materials & Methods:The crude extracts of UTMC 676 and UTMC 919 were prepared from the collection of biological compounds of Tehran University. After cell treatment with UTMC 676 and UTMC 919, cell cytotoxicity, apoptosis, and mRNA expression were measured using MTT, flow cytometry, and q-RT-PCR methods. Doxorubicin was utilized as a positive control. Results:The MTT results showed induction of cytotoxicity by UTMC 676, UTMC 919, and doxorubicin in A549 cells in a concentration-dependent manner. After 48 hours of treatment, both UTMC 676 and UTMC 919 induced apoptosis in the A549 cell line. However, the apoptotic effect of UTMC 676 was more than doxorubicin. The q-RT-PCR data exhibited that the expression of apoptosis-related genes was enhanced in the treated group compared to the untreated group. Conclusion:These results suggest that the crude extract of UTMC 676 was able to induce apoptosis in A549 cells and could be a very promising source having therapeutic potential against lung cancer cell lines.
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.
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