نقش miR-21 به عنوان یک انکوژن واقعی در سرطان پستان
ترجمه نشده

نقش miR-21 به عنوان یک انکوژن واقعی در سرطان پستان

عنوان فارسی مقاله: نقش miR-21 به عنوان یک انکوژن واقعی در واسطه گری مقاومت دارویی در سرطان پستان
عنوان انگلیسی مقاله: Role of miR-21 as an authentic oncogene in mediating drug resistance in breast cancer
مجله/کنفرانس: ژن - Gene
رشته های تحصیلی مرتبط: پزشکی، داروسازی
گرایش های تحصیلی مرتبط: خون و انکولوژی، داروشناسی، ایمنی شناسی، ژنتیک پزشکی، پزشکی مولکولی
کلمات کلیدی فارسی: سرطان پستان، مقاومت دارويی، میکرو آر ان ای، miR-21
کلمات کلیدی انگلیسی: Breast cancer، Drug resistance، microRNA، miR-21
نوع نگارش مقاله: مقاله مروری (Review Article)
نمایه: Scopus - Master Journals List - JCR - MedLine
شناسه دیجیتال (DOI): https://doi.org/10.1016/j.gene.2020.144453
دانشگاه: Immunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran
ناشر: الزویر - Elsevier
نوع ارائه مقاله: ژورنال
نوع مقاله: ISI
سال انتشار مقاله: 2020
ایمپکت فاکتور: 2/708 در سال 2019
شاخص H_index: 164 در سال 2020
شاخص SJR: 0/911 در سال 2019
شناسه ISSN: 0378-1119
شاخص Quartile (چارک): Q1 در سال 2019
فرمت مقاله انگلیسی: PDF
تعداد صفحات مقاله انگلیسی: 14
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: E14786
رفرنس: دارای رفرنس در داخل متن و انتهای مقاله
فهرست انگلیسی مطالب

Abstract


1- Introduction


2- Breast cancer


3- Drug resistance


4- miRNA biogenesis


5- miR-21 in BC


6- Expression of miR-21 in cancer tissues and cells


7- Role of miR-21 as a mediator in drug resistance in BC


8- Upstream pathway of miR-21


9- Potential targets of miR-21


10- Conclusion and future perspectives


References

نمونه متن انگلیسی مقاله

Abstract


Breast cancer (BC) is the most common cancer among women that is responsible for the most of the cancer-related death in worldwide. Drug resistance is remaining as a significant clinical obstacle to treat BC patients effectively. Therefore, to help overcome this problem, it is necessary to understand the mechanisms of drug resistance. microRNAs classify as highly conserved non-coding RNAs (~22 nucleotides) and interact with mRNAs-coding genes for direct post-transcriptional repression. It has been reported that miR-21 is overexpressed and also acts as oncomiR in many human malignancies by targeting of several tumor suppressor genes–associated with apoptosis, proliferation and metastasis. Specifically, it has been reported that miR-21 is responsible for the drug resistance and its overexpression is related to the development of Multi Drug Resistance (MDR) in breast cancer. In this review, we discussed about the role of miR-21 on the drug resistance of breast cancer.


Introduction


Breast cancer (BC) is responsible for the death of approximately 500,000 women per year in the world. Also, more than one million new case of BC is diagnosed across the world per year. The occurrence of BC accounts for 7-8% of the entire number of malignant tumors. Chemotherapy is known as a principal strategy for cancer treatment; however, its application is limited due to drug resistance. Resistance to chemotherapeutics is mainly divided into two extensive categories: (i) intrinsic and (ii) acquired. Intrinsic resistance shows the presence of resistance-mediating factors in the tumor before starting of treatment process that makes chemotherapy ineffective. Acquired drug resistance, however, will be developed during of the treatment [1,2]. Drug resistance brings serious clinical obstacles to the prosperous treatment of BC patients. To overcome these problems, a well understanding of the drug resistance mechanisms is definitely required. The molecular mechanism of chemotherapeutic resistance in BC cells is completely complicated, and comprises multiple processes, including epigenetic changes, gene mutation, gene amplification and microRNA expression. miRNAs are short non-coding RNAs (~22 nucleotides) that could be found in all eukaryotic cells. They have a significant role in the progression of cancer by binding to the 3' untranslated region (UTR) of the target genes, leading to the target mRNA degradation and inhibition of translation.

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