Cytotoxic effects of Zn oxide nanoparticles against breast cancer T47D cells and NM23 gene expression

Background: Breast cancer is the second leading cause of cancer-related death worldwide among women. Nowadays, nanoparticles are interested as anti-cancer factors in studies related to cancer therapy. Therefore, the present study aimed to explore cytotoxic effects of zinc oxide nanoparticles (ZnONPs) and to evaluate NM23 gene expression in T47D breast cancer cells. Materials and Methods: The cancerous T47D and normal HEK293 cell lines were treated with different concentration of ZnONPs for 24 hours and the cytotoxicity activity of ZnONPs was analyzed by the MTT assay. Then, the NM23 gene expression was evaluated using the real-time PCR method. Results: According to MTT results, the ZnONPs significantly decreased the viability of T47D cells in dose-dependent manner. Also, the results revealed that the mRNA level of NM23 was up-regulated (7.8-fold) in cells treated with ZnONPs. Conclusion: ZnONPs can destroy cancerous T47D cells compared to normal HEK293 cells. Furthermore, it seems that ZnONPs can modulate metastasis by enhancing the NM23 gene expression level in breast cancer T47D cells. Thus, ZnONPs can be considered as a promising strategy for the treatment of breast cancer

Cytotoxic effects of Zn oxide nanoparticles against breast cancer T47D cells and NM23 gene expression

Background: Breast cancer is the second leading cause of cancer-related death worldwide among women. Nowadays, nanoparticles are interested as anti-cancer factors in studies related to cancer therapy. Therefore, the present study aimed to explore cytotoxic effects of zinc oxide nanoparticles (ZnONPs) and to evaluate NM23 gene expression in T47D breast cancer cells. Materials and Methods: The cancerous T47D and normal HEK293 cell lines were treated with different concentration of ZnONPs for 24 hours and the cytotoxicity activity of ZnONPs was analyzed by the MTT assay. Then, the NM23 gene expression was evaluated using the real-time PCR method. Results: According to MTT results, the ZnONPs significantly decreased the viability of T47D cells in dose-dependent manner. Also, the results revealed that the mRNA level of NM23 was up-regulated (7.8-fold) in cells treated with ZnONPs. Conclusion: ZnONPs can destroy cancerous T47D cells compared to normal HEK293 cells. Furthermore, it seems that ZnONPs can modulate metastasis by enhancing the NM23 gene expression level in breast cancer T47D cells. Thus, ZnONPs can be considered as a promising strategy for the treatment of breast cancer

Exome sequencing utility in defining the genetic landscape of hearing loss and novel-gene discovery in Iran

Hearing loss (HL) is one of the most common sensory defects affecting more than 466 million individuals worldwide. It is clinically and genetically heterogeneous with over 120 genes causing non-syndromic HL identified to date. Here, we performed exome sequencing (ES) on a cohort of Iranian families with no disease-causing variants in known deafness-associated genes after screening with a targeted gene panel. We identified likely causal variants in 20 out of 71 families screened. Fifteen families segregated variants in known deafness-associated genes. Eight families segregated variants in novel candidate genes for HL: DBH, TOP3A, COX18, USP31, TCF19, SCP2, TENM1, and CARMIL1. In the three of these families, intrafamilial locus heterogeneity was observed with variants in both known and novel candidate genes. In aggregate, we were able to identify the underlying genetic cause of HL in nearly 30% of our study cohort using ES. This study corroborates the observation that high-throughput DNA sequencing in populations with high rates of consanguineous marriages represents a more appropriate strategy to elucidate the genetic etiology of heterogeneous conditions such as HL