کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8525442 | 1557940 | 2018 | 9 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
MicroRNA-132 and microRNA-212 mediate doxorubicin resistance by down-regulating the PTEN-AKT/NF-κB signaling pathway in breast cancer
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کلمات کلیدی
Roswell Park Memorial Institute medium 1640RPMI 1640P-gpMDRBcrpDMEMqRT-PCRTBPROCAUC - AUCDulbecco’s modified Eagle medium - Modified Eagle اصلاح شده DulbeccoMTT - MTTP-glycoprotein - P-گلیکوپروتئینImmunohistochemistry - ایمونوهیستوشیمیIHC - ایمونوهیستوشیمیmiR-132 - به miR-132Breast cancer - سرطان پستانphosphatase and tensin homolog deleted on chromosome ten - فسفاتاز و هومولوگ تنسین حذف شده در کروموزوم دهMulti-drug resistance - مقاومت چند داروییarea under the curve - منطقه تحت منحنیMicroRNA - میکرو RNA quantitative real-time PCR - واکنش زنجیره ای پلیمراز واقعی در زمان واقعیTATA binding protein - پروتئین متصل به TATAbreast cancer resistance protein - پروتئین مقاومت به سرطان سینهPten - ژن PTENnegative control - کنترل منفیreceiver operating characteristic - گیرنده عامل عامل
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
تومور شناسی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Breast cancer is a serious health problem worldwide. Acquisition of multi-drug resistance (MDR) during the treatment of breast cancer is still considered a major clinical obstacle. Despite the biological functions of miRNAs becoming increasingly apparent, the function of miRNAs in regulating drug resistance of breast cancer remains under investigation. Quantitative real-time PCR (qRT-PCR) was used to quantify the expression of miR-132/-212 (miR-132 and miR-212) in doxorubicin (DOX)-resistant and -sensitive breast cancer tumors and cells. The function of miR-132/-212 in drug resistance was investigated in vitro (MTT assay, TUNEL assay, fluorescence, immunohistochemistry, luciferase reporter assay, Western blotting). We found that miR-132/-212 were commonly overexpressed in DOX-resistant breast cancer tumors and cells. Silenced miR-132/-212 expression induced DOX accumulation in MCF-7/ADR cells, while overexpression of miR-132/-212 led to breast cancer resistance protein (BCRP)-based DOX efflux in MCF-7 cells. Further study showed that up-regulation of miR-132/-212 in MCF-7/ADR cells suppressed the expression of PTEN, a target gene of miR-132/-212, which activated AKT phosphorylation and the NF-κB pathway and led to increased BCRP expression. Down-regulation of miR-132/-212 sensitized MCF-7/ADR cells to DOX. Mechanistic investigations suggested that miR-132/-212 enhancement was a result of NF-κB-mediated transactivation of the pri-miR-132/-212 gene. Taken together, our findings are among the first to demonstrate a novel aspect of the miR-132/-212-PTEN-AKT/NF-κB-BCRP pathway in the generation of breast cancer resistance and provides a potential method to reverse drug resistance.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biomedicine & Pharmacotherapy - Volume 102, June 2018, Pages 286-294
Journal: Biomedicine & Pharmacotherapy - Volume 102, June 2018, Pages 286-294
نویسندگان
Manxin Xie, Ziyi Fu, Jianxiang Cao, Yuan Liu, Jie Wu, Qing Li, Yun Chen,