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Analysis of Expression Profiles of GLI3A, LATS2 and MOB1A genes in Patients with Congenital hypothyroidism | ||
Journal of Epigenetics | ||
دوره 3، شماره 1، خرداد 2022، صفحه 21-26 اصل مقاله (301.86 K) | ||
نوع مقاله: Original Article | ||
شناسه دیجیتال (DOI): 10.22111/jep.2022.38960.1029 | ||
نویسندگان | ||
Sepideh Eisazaei1؛ Maryam Nakhaee-Moghadam* 2؛ Dor-Mohammad Kordi Tamandani3 | ||
1Department of Biology, Faculty of Sciences, University of Sistan and Baluchestan, Zahedan, Iran. | ||
2Pediatric, Children and Adolescents health Researche Center, Resistant Tuberculosis Institute, Zahedan University of Medical Sciences, Zahedan, Iran. | ||
3Department of Biology, Faculty of Sciences, University of Sistan and Baluchestan, Zahedan, | ||
چکیده | ||
In recent years, congenital hypothyroidism (CH) has been reported as the most prevalent endocrine disorder and most common cause of preventable mental retardation in many parts of the world, especially in Asia. Delays in early diagnosis and treatment of CH can lead to growth retardation, as well as neurological and psychological disorders. Many genetic defects along with their molecular mechanisms based on pathophysiology have not been identified in many babies with congenital hypothyroidism. This study aimed to evaluate the expression of GLI3A and LATS2, MOB1A genes in patients with congenital hypothyroidism. In this study, the expression pattern of GLI3A, LATS2, and MOB1A genes after RNA extraction and converted to cDNA from the blood of 20 patients and 20 control samples were examined by the Real-time quantitative PCR (qRT-PCR). The obtained data were analyzed using Spss software and Mann-Whitney statistical method. Statistical analysis of findings has shown significant differences in the expression of GLI3A gene in two groups of patients and control. However, in the study on the expression of two genes LATS2 and MOB1A, there was no significant difference, so it can be assumed that expression of GLI3A gene may play a role in risk of congenital hypothyroidism while changes in expression of LATS2 and MOB1A genes are not involved in this disease. Results of the present study demonstrated that GLI3A gene expression could be a genetic risk factor for congenital hypothyroidism. In the present study, LATS2 and MOB1A gene expression did not show significant risk for susceptibility CH disease. | ||
کلیدواژهها | ||
Expression؛ GLI3A؛ MOB1A؛ LATS2؛ Congenital hypothyroidism؛ Real-time PCR | ||
مراجع | ||
Bajracharya, L. (2019). Neonatal thyroid screening for congential hypothyroidism. Journal of Diabetes and Endocrinology Association of Nepal. 3, 32-33.
Bona, G., De Luca, F., & Monzani, A. (2015). Thyroid diseases in childhood: recent advances from basic science to clinical practice: spring.
Büyükgebiz, A. (2013). Newborn screening for congenital hypothyroidism. hypothyroidism. Journal of clinical research in pediatric endocrinology, 5, 8.
Carballo, G. B., Honorato, J. R., & de Lopes, G. P. F. (2018). A highlight on Sonic hedgehog pathway. Communication and Signaling. 16, 11.
Delange, F. (1997). Neonatal screening for congenital hypothyroidism: results and perspectives. Hormones. 48, 51-61
Dorreh, F., Chaijan, P. Y., Javaheri, J., & Zeinalzadeh, A. H. (2014). Journal of clinical research in pediatric endocrinology. J. clin. Res. Pediatr. Endocrinol. 6, 105.
Ehmer, U., & Sage, J. (2016). Control of proliferation and cancer growth by the Hippo signaling pathway. Molecular Cancer Research. 14, 127-140.
Furth, N., & Aylon, Y. (2017). The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway. Cell Death & Differentiation. 24, 1488-1501.
Fisher, D. A., Dussault, J. H., Foley Jr, T. P., Klein, A. H., LaFranchi, S., Larsen, P. R., ... & Walfish, P. G. (1979). Screening for congenital hypothyroidism: results of screening one million North American infants. The Journal of pediatrics. 94, 700-705.
Fagman, H., Grände, M., et al. (2004). Genetic deletion of sonic hedgehog causes hemiagenesis and ectopic development of the thyroid in mouse. The American journal of pathology. 164, 1865-1872.
Fagman, H., Grände, M., Gritli-Linde, A., & Nilsson, M. (2014). Developmental hypothyroxinemia and hypothyroidism reduce proliferation of cerebellar granule neuron. Molecular neurobiology. 49.3: 1143-1152.
Fu, C., Luo, S., Long, X., Li, Y., She, S., Hu, X., ... & Su, J. (2018). Mutation screening of the GLIS3 gene in a cohort of 592 Chinese patients with congenital hypothyroidism. Clinica Chimica Acta. 476, 38-43.
Grove, E. A., Tole, S., Limon, J., Yip, L. W., & Ragsdale, C. W. (1998). The hem of the embryonic cerebral cortex is defined by the expression of multiple Wnt genes and is compromised in Gli3-deficient mice. Development. 125, 2315-2325.
Gholami, M., Mirfakhraie, R., & Movafagh, A. (2014). The expression analysis of LATS2 gene in de novo AML patients. Medical Oncology . 2–5.
Hashemipour, M., Samei, P., Kelishadi, R., Hovsepian, S., & Hani Tabaei Zavareh, N. (2019). A systematic review on the risk factors of congenital hypothyroidism. Journal of Pediatrics Review. 7, 199-210.
Hansen, C. G., Moroishi, T., & Guan, K. L. 2015. YAP and TAZ: a nexus for Hippo signaling and beyond. Trends in cell biology. 25, 499-513.
i Altaba, A.R. (1999). Gli proteins and Hedgehog signaling: development and cancer. Trends in genetics. 15, 418-425.
Jetten, A.M. (2018). GLIS1–3 transcription factors: critical roles in the regulation of multiple physiological processes and diseases. Cellular and Molecular Life Sciences. 75, 3473-3494.
Kwak, M. (2018). Clinical genetics of defects in thyroid hormone synthesis. Annals of Pediatric Endocrinology & Metabolism. 23, 169.
Lania, A., Persani, L., & Beck-Peccoz, P. (2008). Central hypothyroidism. Pituitary. 11.2: 181-186.
LaFRANCHI, S. T. E. P. H. E. N. (1999). Congenital hypothyroidism: etiologies, diagnosis, and management. Thyroid. , 9.7: 735-740.
Lee, H. H., Vo, M. T., Kim, H. J., Lee, U. H., Kim, C. W., Kim, H. K., ... & Choi, D. H. (2010). Stability of the LATS2 tumor suppressor gene is regulated by tristetraprolin. Journal of Biological Chemistry. 285, 17329-17337.
Nakajima, M., Tsuchiya, K., Fukuda, S., Morimoto, H., Mitsumori, Y., & Kato, K. (2006). Aortic operation after previous coronary artery bypass grafting. General Thoracic and Cardiovascular Surgery. Card Sur. 54, 155-159.
Niewiadomski, P., Niedziółka, S. M., Markiewicz, Ł., Uśpieński, T., Baran, B., & Chojnowska, K. (2019). Gli proteins: Regulation in development and cancer. Cells. 8, 147.
Nilsson, M., & Fagman, H. (2017). Development of the thyroid gland. Development. 144, 2123-2140.
Nishio, M., Hamada, K., Kawahara, K., Sasaki, M., Noguchi, F., Chiba, S., ... & Morikawa, T. (2012). Cancer susceptibility and embryonic lethality in Mob1a/1b double-mutant mice. The Journal of clinical investigation. 122, 4505-4518.
Ou, C., Sun, Z., Li, S., Li, G., Li, X., & Ma, J. (2017). Dual roles of yes-associated protein (YAP) in colorectal cancer. Oncotarget. 8, 75727
Pardo Campos, M. L., Musso, M. F., Keselman, A., Gruñeiro, L., Bergadá, I., & Chiesa, A., (2017). Cognitive profiles of patients with early detected and treated congenital hypothyroidism. Arch Argent Pediatr. 115, 12-17
Park, S. M., & Chatterjee, V. K. K. (2005). Genetics of congenital hypothyroidism. Journal of medical genetics. 42, 379-389.
Wang, Y., Wang, Y., Dong, J., Wei, W., Song, B., Min, H., ... & Chen, J. (2014). Developmental hypothyroxinemia and hypothyroidism reduce proliferation of cerebellar granule neuron precursors in rat offspring by downregulation of the sonic hedgehog signaling pathway. Molecular neurobiology, 49(3), 1143-1152.
Pinosa, F., Begheldo, M., Pasternak, T., Zermiani, M., Paponov, I. A., Dovzhenko, A., ... & Palme, K. (2013). The Arabidopsis thaliana Mob1A gene is required for organ growth and correct tissue patterning of the root tip. Annals of botany. 112, 1803-1814.
Rastogi, M. V., & LaFranchi, S. H. (2010). Congenital hypothyroidism. Orphanet journal of rare diseases. 5, 17.
Rimkus, T. K., Carpenter, R. L., Qasem, S., Chan, M., & Lo, H. W. (2016). Targeting the sonic hedgehog signaling pathway: review of smoothened and GLI inhibitors. Cancers. 8, 22.
Szinnai, G. (2014). Clinical genetics of congenital hypothyroidism. Paediatric Thyroidology. 26, 60-78.
Sabol, M., Trnski, D., Musani, V., Ozretić, P., & Levanat, S. (2018). Role of GLI transcription factors in pathogenesis and their potential as new therapeutic targets. International journal of molecular sciences. 19, 2562.
Shi, Y., Geng, D., Zhang, Y., Zhao, M., Wang, Y., Jiang, Y., & Yu, R. (2019). LATS2 Inhibits Malignant Behaviors of Glioma Cells via Inactivating YAP. Journal of Molecular Neuroscience. 68.1: 38-48.
Torres-Manzo, P., Cano-Europa, E., Blas-Valdivia, V., Franco-Colin, M., & Ortiz-Butron, R. (2014). Hypothyroidism: Diagnosis and Screening, Genetic Influences, and Treatment Options. Clinical and Experimental Medical Sciences. 2, 11-47
Wassner, A.J. 2018. Congenital hypothyroidism. Clinics in perinatology. 45, 1-18.
Waller, D. K., Anderson, J. L., Lorey, F., & Cunningham, G. C. (2000). Risk factors for congenital hypothyroidism: an investigation of infant's birth weight, ethnicity, and gender in California, 1990–1998. Teratology. 62, 36-41.
Zhang, R., Zhang, H., Zhu, W., Pardee, A. B., Co, R. J., & Liang, P. (1997). Mob-1 , a Ras target gene , is overexpressed in colorectal cancer. Oncogene. 14.13: 1607-1610. | ||
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