کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10914564 | 1088794 | 2016 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
ÎNp63α induces quiescence and downregulates the BRCA1 pathway in estrogen receptor-positive luminal breast cancer cell line MCF7 but not in other breast cancer cell lines
دانلود مقاله + سفارش ترجمه
دانلود مقاله ISI انگلیسی
رایگان برای ایرانیان
کلمات کلیدی
TNBCCTCDOXBCSCDTCp63IPAIngenuity Pathway Analysis - تجزیه و تحلیل راه Ingenuityquiescence - خستگیDormancy - خُفتگیdoxycycline - داکسی سایکلینTriple negative breast cancer - سرطان سینه سه گانه منفیbasal-like breast cancer - سرطان سینه پایه مانندBreast cancer - سرطان پستانStem cell - سلول بنیادیBreast cancer stem cell - سلول بنیادی سرطان پستانdisseminated tumor cell - سلول تومور منتشر شده استBMP - مدیریت فرایند کسب و کارGene ontology - هستیشناسی ژنیBone morphogenetic protein - پروتئین مورفوژنیک استخوانcirculating tumor cell - گردش سلول تومورEstrogen receptor - گیرنده استروژن
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
تحقیقات سرطان
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: ÎNp63α induces quiescence and downregulates the BRCA1 pathway in estrogen receptor-positive luminal breast cancer cell line MCF7 but not in other breast cancer cell lines ÎNp63α induces quiescence and downregulates the BRCA1 pathway in estrogen receptor-positive luminal breast cancer cell line MCF7 but not in other breast cancer cell lines](/preview/png/10914564.png)
چکیده انگلیسی
Despite apparent resection of tumors, breast cancer patients often suffer relapse due to remnant dormant tumor cells. Although quiescence of cancer stem cells is thought as one of the mechanisms regulating dormancy, the mechanism underlying quiescence is unclear. Since ÎNp63α, an isoform of p51/p63, is crucial in the maintenance of stem cells within mammary epithelium, we investigated its roles in the regulation of dormancy in normal and malignant breast cells. Inducible expression of ÎNp63α in MCF7 estrogen receptor positive (ER+) luminal breast cancer cells led to quiescence and acquisition of progenitor-like properties. Judging from mRNA-microRNA microarray analysis, activation of bone morphogenetic protein (BMP) signaling and inhibition of Wnt signaling emerged as prominent mechanisms underlying ÎNp63α-dependent induction of quiescence and acquisition of stemness in MCF7. More interestingly, through Ingenuity Pathway analysis, we found for the first time that BRCA1 pathway was the most significantly downregulated pathway by ÎNp63α expression in quiescent MCF7 cells, where miR-205 was a downstream mediator. Furthermore, ÎNp63α-expressing MCF7 cells exhibited resistance to paclitaxel and doxorubicin. Expression of ÎNp63α in normal MCF10A basal cells increased proliferation and stemness, but did not affect more aggressive luminal (T47D) and basal (MDA-MB-231) cells with p53 mutation. Gene expression datasets analyses suggested that ÎNp63 expression is associated with relapse-free survival of luminal A/B-type patients, but not of the other subtypes. Our results established a cell type-specific function of ÎNp63α in induction of quiescence and downregulation of the BRCA1 pathway which suggested a role of ÎNp63α in the dormancy of luminal breast cancers.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Molecular Oncology - Volume 10, Issue 4, April 2016, Pages 575-593
Journal: Molecular Oncology - Volume 10, Issue 4, April 2016, Pages 575-593
نویسندگان
Ruhul Amin, Yuiko Morita-Fujimura, Hiroshi Tawarayama, Kentaro Semba, Natsuko Chiba, Manabu Fukumoto, Shuntaro Ikawa,