Dr. Sadeq Vallian Boroujeni received his Bachelor's degree (BSc.) in Genetics from Ahvaz Jundishapur University (Shahid Chamran) and a Master's degree (MSc.) in Clinical Biochemistry from Isfahan University of Medical Sciences. He then completed his doctoral level at the University of London, England, the School of Medicine and Dentistry (King's College) in the field of Molecular Medicine. Then he completed his post-doctoral fellowship in the Department of Laboratory Medicine of MD Anderson Cancer Centre at University of Texas, USA. Since 1379, he has been working as a faculty member at the University of Isfahan. In 2012, he was awarded the full degree of professor and is now teaching and researching in the Genetics Division of the Department of Molecular and Cellular Biology and Microbiology this university.
His main research involves molecular study and diagnosis of genetic diseases and cancer, especially:
A) Study and identification of drug resistance markers in blood and breast cancers
B) Identification of mutations related to genetic diseases in the population of Iran
ِDr Vallian's main research involves molecular study and diagnosis of genetic diseases and cancer, especially:
A) Study and identification of drug resistance markers in blood and breast cancers
B) Identification of mutations related to genetic diseases in the population of Iran
Articles
Scientific Reports (20452322)14(1)
Correction to: Scientific Reportshttps://doi.org/10.1038/s41598-023-49155-5, published online 10 December 2023 The original version of this Article contained an error in Reference 9, which was incorrectly given as: Piryaei, F. et al. Global analysis in non-obstructive azoospermic testis identifies miRNAs critical to spermatogenesis. Andrologia1, 1 (2022). The correct reference is listed below: Piryaei, F. et al. Global analysis in nonobstructive azoospermic testis identifies miRNAs critical to spermatogenesis. Andrologia2023, Article ID 2074931 (2023). https://doi.org/10.1155/2023/2074931. The original Article has been corrected. © The Author(s) 2024.
PLoS ONE (19326203)18(8 August)
Autosomal recessive non-syndromic hearing loss (ARNSHL) is a public health concern in the Iranian population, with an incidence of 1 in 166 live births. In the present study, the whole exome sequencing (WES) method was applied to identify the mutation spectrum of NSHL patients negative for GJB2 gene mutations. First, using ARMS PCR followed by Sanger sequencing of the GJB2 gene, 63.15% of mutations in patients with NSHL were identified. Among the identified mutations in GJB2:p.Val43Met and p.Gly21Arg were novel. The remaining patients were subjected to WES, which identified novel mutations including MYO15A:p.Gly39LeufsTer188, ADGRV1:p.Ser5918ValfsTer23, MYO7A: c.5856+2T>c (splicing mutation), FGF3:p.Ser156Cys. The present study emphasized the application of WES as an effective method for molecular diagnosis of NSHL patients negative for GJB2 gene mutations in the Iranian population. © 2023 Broojeni et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Scientific Reports (20452322)13(1)
MiR-34b-5p has been reported as a non-invasive diagnostic biomarker for infertility. However, no gene targets regulating the mechanism of cation of this miRNA are known. In this study, using gene set enrichment analysis the Inositol 1,4,5-Trisphosphate Receptor Type 1 (ITPR1) gene was identified as the sole target for hsa-miR-34b-5p, and found significantly overexpressed in non-obstructive azoospermia (NOA) patients. This finding was confirmed by qRT-PCR on fresh testicular tissues from NOA patients. Then, pathway enrichment analysis as well as the diagnostic value analysis of hsa-miR-34b-5p/ITPR1 indicated ITPR1 as a hub gene in the calcium (Ca2+)-apoptosis pathway, and a valuable predictive biomarker for NOA. Moreover, gene expression and histological assays showed the association of the effects of ITPR1’s increased expression on spermatogenesis failure through induction of apoptosis in NOA patients. These data suggested that the hsa-miR-34b-5p/ITPR1 axis could serve as a potential regulatory predictive biomarker for human spermatogenesis through the Ca2+-apoptosis pathway cross-talk. © 2023, The Author(s).
Molecular Biology Reports (03014851)50(1)pp. 517-530
Background: Myocardial infarction-associated transcript (MIAT) is a long non-coding RNA (lncRNA) with altered expression in different diseases and malignancies. In this study, the potential expression and function of lncRNA MIAT in intuition and progression of brain cancer was investigated. Methods and Results: At first, TCGA data analysis demonstrated that lncRNA MIAT is significantly upregulated in various malignancies, especially its expression is dramatically elevated in brain tumors. In line with the data, we further evaluated the expression of MIAT in a series of brain tumor tissue, and our results revealed that the expression of MIAT was noticeably overexpressed in glioblastoma (p = < 0.0001). We further found that the expression of MIAT was markedly upregulated in low-grade brain tumors rather than high-grade ones. To further investigate the biological function of MIAT in brain cancer cells, its expression was suppressed by si-RNA-mediated knocking down. Inhibition of MIAT resulted in reduced proliferation of brain tumor cells followed by cell cycle arrest at the G1 phase, and significant induction of apoptosis, and senescence, but limited the migration ability and epithelial-mesenchymal-transition (EMT). Moreover, knocking-down of MIAT reduced the expression of stemness factors, followed by upregulation of their downstream miRNAs (micro RNAs), let-7a-5p, and miR-29b-3p. Conclusions: Altogether, our data demonstrated that lncRNA MIAT could control proliferation, migration, and metastasis of brain cancer cells via regulating the Nanog/ Sox2 / let-7a-5p / miR-29b-3p axis. This data could introduce lncRNA MIAT as a novel oncogene in brain cancer pathogenesis. © 2022, The Author(s), under exclusive licence to Springer Nature B.V.
