کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8258473 | 1534608 | 2018 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Androgen deprivation therapy-induced epithelial-mesenchymal transition of prostate cancer through downregulating SPDEF and activating CCL2
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کلمات کلیدی
ADTNEPCCRPCTCGAGSEACSSSPDEFRT-PCRNeuroendocrine prostate cancerGFPFDRMFIDHTNSECCL2FACSThe cancer genome atlas - اوتومتر ژنوم سرطانchromatin immunoprecipitation - ایمن سازی کروماتینImmunofluorescence - ایمونوفلورسانسimmunohistochemical - ایمونوهیستوشیمیIHC - ایمونوهیستوشیمیGene Set Enrichment Analysis - تجزیه و تحلیل غنی سازی مجموعه ژنیTRAMP - ترامپEMT - تکنسین فوریتهای پزشکیAndrogen-deprivation therapy - درمان آندروژن محرومfluorescence-activated cell sorting - دسته بندی سلول های فعال فلورسنسDihydrotestosterone - دی هیدروتستوسترونFluorescent intensity - شدت فلورسنتphosphatase and tensin homolog - فسفاتاز و تنسین همولوگfalse discovery rate - میزان کشف کاذبnormalized enrichment score - نمره غنی سازی نرمال شدهreal-time quantitative polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استgreen fluorescent protein - پروتئین فلورسنت سبزCHiP - چیپPten - ژن PTENepithelial-to-mesenchymal transition - گذار اپیتلیال به مزانشیمالAndrogen Receptor - گیرنده آندروژنی
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
سالمندی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The chemokine CC motif ligand 2 (CCL2) is important in recruiting tumor-associated macrophages and is involved in the development of castration-resistance prostate cancer (CRPC) after androgen-deprivation therapy (ADT); however, the underlying mechanism remains unclear. We found that inactivation of the androgen receptor (AR) reduces a transcriptional repressor (SAM pointed domain-containing ETS transcription factor, SPDEF) of CCL2, which mediates epithelial-to-mesenchymal transition (EMT) of prostate tumor cells. Cell lines derived from a prostate-specific Pten/Trp53-null mouse and capable of a spontaneous EMT were utilized for identification of CCL2, and showed that reduced SPDEF expression was associated with an elevated CCL2-activated EMT. AR signaling inhibits CCL2 through a SPDEF-mediated mechanism in that the SPDEF recognizes the CCL2 promoter and transcriptionally represses its activity. Ectopically expressed SPDEF reduced the EMT and rescued expression of CCL2 in SPDEF-expressing cells, which induced the EMT and promotes malignant functions of prostate cancer cells. In tissues from prostate cancer patients with ADT, low SPDEF levels were correlated with high CCL2 expression compared to patients without ADT. We present a novel mechanism that contributes to the EMT and metastatic phenotype observed in a subset of ADT-resistant prostate cancer, where the CCL2 is stimulated through the inactivated of AR-mediated SPDEF.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 5, Part A, May 2018, Pages 1717-1727
Journal: Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease - Volume 1864, Issue 5, Part A, May 2018, Pages 1717-1727
نویسندگان
Yuan-Chin Tsai, Wei-Yu Chen, Wassim Abou-Kheir, Tao Zeng, Juan Juan Yin, Hisham Bahmad, Yi-Chao Lee, Yen-Nien Liu,