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LncRNA Miat Promotes Proliferation of Cervical Cancer Cells and Acts as an Anti-apoptotic Factor | ||
| Journal of Genetic Resources | ||
| مقاله 2، دوره 3، شماره 2، آذر 2017، صفحه 80-86 اصل مقاله (768.34 K) | ||
| نوع مقاله: Research Article | ||
| شناسه دیجیتال (DOI): 10.22080/jgr.2018.13369.1079 | ||
| نویسندگان | ||
| Firooz Jannat Alipoor؛ Malek Hossein Asadi* ؛ Masoud Torkzadeh-Mahani | ||
| Department of Biotechnology, Institute of Science and High Technology and Environmental Sciences, Graduate University of Advanced Technology, Kerman, Iran | ||
| تاریخ دریافت: 26 تیر 1396، تاریخ بازنگری: 25 دی 1396، تاریخ پذیرش: 06 شهریور 1396 | ||
| چکیده | ||
| There are a sub-population of cells in tumor tissues known as cancer stem cells (CSCs) which have similar features with stem cells, including self-renewal and differentiation capacity. Recently, it was established that not only stem cells factors such as Oct4, but also ES-associated lncRNAs are contributing to various regulatory aspects of CSCs. Myocardial infarction associated transcript (MIAT) is a lncRNA which expressed in embryonic stem cells (ESCs) and its expression was regulated by ES-associated transcription factors, Oct4 and Nanog. Here, our results revealed that suppression of MIAT reduces cell proliferation and causes G1 arrest in HeLa cancer cells through downregulation of cell cycle progression factors including, CyclinD1 and PCNA. Furthermore, our data showed that downregulation of MIAT represses migration of HeLa cells which implicated that MIAT may be contributed to the migration of HeLa cells. We further detected MIAT silencing promotes apoptosis of Hela cancer cells and influences the expression of known apoptotic factors, Bcl2 and Bax. Based on our findings, LncRNA MIAT might be involved in the cervical cancer malignant progression and it could be the candidate as a potential therapeutic target to combat cancer. | ||
| کلیدواژه‌ها | ||
| LncRNA MIAT؛ Cervical cancer؛ G1 arrest؛ Apoptosis | ||
| مراجع | ||
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