نقش SOX2 در توسعه و زیست شناسی سرطان
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نقش SOX2 در توسعه و زیست شناسی سرطان

عنوان فارسی مقاله: SOX2 در توسعه و زیست شناسی سرطان
عنوان انگلیسی مقاله: SOX2 in development and cancer biology
مجله/کنفرانس: سمینارهای زیست شناسی سرطان - Seminars In Cancer Biology
رشته های تحصیلی مرتبط: پزشکی، زیست شناسی
گرایش های تحصیلی مرتبط: پزشکی مولکولی، ایمنی شناسی پزشکی، علوم سلولی و مولکولی، خون و انکولوژی
کلمات کلیدی فارسی: سرطان، Sox2، توسعه، تومور، سلول بنیادی
کلمات کلیدی انگلیسی: Cancer، Sox2، Development، Tumor، Stem cell
نوع نگارش مقاله: مقاله مروری (Review Article)
نمایه: Master ISC - MedLine - Scopus - Master Journals List - JCR
شناسه دیجیتال (DOI): https://doi.org/10.1016/j.semcancer.2019.08.007
دانشگاه: Skin Cancer Unit, German Cancer Research Center (DKFZ), Heidelberg, Germany
ناشر: الزویر - Elsevier
نوع ارائه مقاله: ژورنال
نوع مقاله: ISI
سال انتشار مقاله: 2019
ایمپکت فاکتور: 8/752 در سال 2018
شاخص H_index: 134 در سال 2019
شاخص SJR: 3/259 در سال 2018
شناسه ISSN: 1044-579X
شاخص Quartile (چارک): Q1 در سال 2018
فرمت مقاله انگلیسی: PDF
تعداد صفحات مقاله انگلیسی: 9
وضعیت ترجمه: ترجمه نشده است
قیمت مقاله انگلیسی: رایگان
آیا این مقاله بیس است: خیر
آیا این مقاله مدل مفهومی دارد: ندارد
آیا این مقاله پرسشنامه دارد: ندارد
آیا این مقاله متغیر دارد: ندارد
کد محصول: E13024
رفرنس: دارای رفرنس در داخل متن و انتهای مقاله
فهرست انگلیسی مطالب

Abstract


1- Introduction


2- SOX2 in development


3- The role of SOX2 in embryonic and adult stem cells


4- The role of SOX2 in disease and cancer


5- Conclusions and future perspectives


References

نمونه متن انگلیسی مقاله

Abstract


The transcription factor SOX2 is essential for embryonic development and plays a crucial role in maintaining the stemness of embryonic cells and various adult stem cell populations. On the other hand, dysregulation of SOX2 expression is associated with a multitude of cancer types and it has been shown that SOX2 positively affects cancer cell traits such as the capacity to proliferate, migrate, invade and metastasize. Moreover, there is growing evidence that SOX2 mediates resistance towards established cancer therapies and that it is expressed in cancer stem cells. These findings indicate that studying the role of SOX2 in the context of cancer progression could lead to the development of new therapeutic options. In this review, the current knowledge about the role of SOX2 in development, maintenance of stemness, cancer progression and the resistance towards cancer therapies is summarized.


Introduction


In 1990, a new transcription factor with a distinctive DNA-binding domain was described to be involved in testis determination. The gene encoding for this protein was found to be located on the sex-determining region of the Y chromosome and was therefore termed sexdetermining region Y (SRY) gene [1,2]. The Sry protein binds to specific DNA sequences with its high-mobility-group (HMG) domain. Since its discovery a new gene family has been established on the basis of sequence similarities to this HMG domain (Fig. 1). The so-called Sry-related HMG box (SOX) proteins contain an HMG domain with at least 50% sequence similarity to the HMG domain of Sry. Up to the present day, 20 different SOX genes have been found in the murine and human genome which in turn have been divided into eight subgroups based on sequence identity and similar functions [3,4]. In this review, we will focus on SOX2, a member of the SOXB1 subgroup. Among all SOX genes, SOX2 is probably the most recognized due to its role in reprogramming somatic cells into induced pluripotent stem cells (iPSCs) [5]. The human SOX2 gene is situated on chromosome 3 at the position q26.3–27 and encodes for a protein of 317 amino acids [6]. The structural centerpiece of SOX2 is its HMG domain that is highly conserved among species. Apart from binding to specific DNA consensus sequences, this domain also contains a nuclear localization and a nuclear export signal. The function of the C-terminal transactivation domain is to recognize and bind the promoters of target genes and by doing so activating or repressing gene expression [7].

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