کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
10799034 | 1054222 | 2015 | 13 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Cohesin modulates transcription of estrogen-responsive genes
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کلمات کلیدی
cyclin G2RPL13ARNAPIICdLSFoxA1BMPR2cohesinERBBIL-20SOX4Irs2DKK1GATA3PIM2CXCL12BAG1bone morphogenetic protein receptor type IIPI3KThbs1EREGAPDHribosomal protein L13AmTORRNA polymerase II - آرانای پلیمراز II Tff - TFFchromatin immunoprecipitation - ایمن سازی کروماتینInterleukin-20 - اینترلوکین -20Insulin receptor substrate 2 - بستر گیرنده انسولین 2TAD - بلهthrombospondin 1 - ترومبوسپوندن 1topologically associated domain - دامنه مرتبط با توپولوژیTranscription - رونویسیBreast cancer - سرطان پستانCornelia de Lange Syndrome - سندرم کرنلیا د لانگهtrefoil factor - عامل تراکمestrogen response element - عنصر پاسخ استروژنphosphoinositide 3-kinase - فسفینوزیتید 3-کینازmammalian target of rapamycin - هدف پستانداران رپامایسینGATA binding protein 3 - پروتئین گیرنده GATA 3CHiP - چیپChromatin - کروماتینglyceraldehyde 3-phosphate dehydrogenase - گلیسرولیدید 3-فسفات دهیدروژنازEstrogen receptor alpha - گیرنده استروژن آلفاEpidermal growth factor receptor - گیرنده فاکتور رشد اپیدرمال
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The cohesin complex has essential roles in cell division, DNA damage repair and gene transcription. The transcriptional function of cohesin is thought to derive from its ability to connect distant regulatory elements with gene promoters. Genome-wide binding of cohesin in breast cancer cells frequently coincides with estrogen receptor alpha (ER), leading to the hypothesis that cohesin facilitates estrogen-dependent gene transcription. We found that cohesin modulates the expression of only a subset of genes in the ER transcription program, either activating or repressing transcription depending on the gene target. Estrogen-responsive genes most significantly influenced by cohesin were enriched in pathways associated with breast cancer progression such as PI3K and ErbB1. In MCF7 breast cancer cells, cohesin depletion enhanced transcription of TFF1 and TFF2, and was associated with increased ER binding and increased interaction between TFF1 and its distal enhancer situated within TMPRSS3. In contrast, cohesin depletion reduced c-MYC mRNA and was accompanied by reduced interaction between a distal enhancer of c-MYC and its promoters. Our data indicates that cohesin is not a universal facilitator of ER-induced transcription and can even restrict enhancer-promoter communication. We propose that cohesin modulates transcription of estrogen-dependent genes to achieve appropriate directionality and amplitude of expression.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms - Volume 1849, Issue 3, March 2015, Pages 257-269
Journal: Biochimica et Biophysica Acta (BBA) - Gene Regulatory Mechanisms - Volume 1849, Issue 3, March 2015, Pages 257-269
نویسندگان
Jisha Antony, Tanushree Dasgupta, Jenny M. Rhodes, Miranda V. McEwan, Cristin G. Print, Justin M. O'Sullivan, Julia A. Horsfield,