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 and Aims: Congenital heart defects (CHD) are the most common type of congenital disability. Copy number variations (CNVs) have been found as one of the genetic etiology of non-syndromic CHD, and researchers have detected several pathogenic CNVs in patients with cardiac defects. Materials and Methods: In the present study, 70 patients with familial (20 patients) and sporadic (50 patients) non-syndromic CHD were evaluated to find whether CNVs in the GATA4, NKX2-5, TBX-5, CREL, BMP4 genes, and 22q11.2 region contribute to the pathogenesis of non-syndromic CHD. We have used the Multiplex Ligation-dependent Probe Amplification (MLPA) technique as a molecular method to identify CNVs in predefined loci. Results: Normal MLPA results were demonstrated for GATA4, NKX2-5, TBX-5, CRELD, and BMP4 genes for all sporadic and familial cases. However, we found three patients with imbalances for the 22q11.2 region. One patient with 22q11.2 deletion showed tetralogy of fallot, and the other had ventricular septal defects/ pulmonary atresia/ multiple aortopulmonary collateral arteries. A duplication of the 22q11.2 region was detected in one patient with patent ductus arteriosus. Conclusion: Identifying genomic imbalances in 6% of the non-syndromic sporadic patients indicates that recurrent CNVs could be associated with non-syndromic CHD. It seems that it is the first CNV analysis using MLPA carried out in Iranian patients with cardiac defects. We suggest that 22q11.2 imbalances should be considered in patients with cardiac lesions to provide an accurate diagnosis and appropriate genetic counseling in affected families.
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