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305909 occurrences (No.73 in the rank) during 5 years in the PubMed. [cache]
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305909 occurrences (No.73 in the rank) during 5 years in the PubMed. [cache]
| 233) To identify novel markers of AI responsiveness, a genome-wide microarray analysis was performed using primary breast tumor samples from 50 postmenopausal women who later developed metastatic breast cancer. |
| PMID:24413080 DOI:10.1038/onc.2013.553 |
| 2015 Oncogene |
| * Estrogen-dependent sushi domain containing 3 regulates cytoskeleton organization and migration in breast cancer cells. |
| - Aromatase inhibitors (AIs) are the standard endocrine therapy for postmenopausal breast cancer; however, currently used biomarkers, such as, estrogen receptor-alpha/progesterone receptor (ERα/PR), predict only slightly more than half of the potential responders to AI treatment. To identify novel markers of AI responsiveness, a genome-wide microarray analysis was performed using primary breast tumor samples from 50 postmenopausal women who later developed metastatic breast cancer. Sushi domain containing 3 (SUSD3) is a significantly differentially expressed gene, with 3.38-fold higher mRNA levels in AI-responsive breast tumors vs non-responders (P<0.001). SUSD3 was highly expressed in ERα-positive breast tumors and treatment with estradiol increased SUSD3 expression in ERα-positive breast cancer cells. Treatment with an antiestrogen or ERα knockdown abolished basal and estradiol-dependent SUSD3 expression. Recruitment of ERα upstream of the transcription start site of SUSD3 was demonstrated by chromatin immunoprecipitation-PCR. Flow cytometric analysis of SUSD3-knockdown cells revealed blunted estradiol effects on progression into S and M phases. SUSD3 was localized to the plasma membrane of breast cancer cells. SUSD3 knockdown decreased the appearance of actin-rich protrusions, stress fibers and large basal focal adhesions, while increasing the presence of cortical actin concomitant with a decrease in Rho and focal adhesion kinase activity. SUSD3-deficient cells demonstrated diminished cell spreading, cell-cell adhesion and motility. In conclusion, SUSD3 is a novel promoter of estrogen-dependent cell proliferation and regulator of cell-cell and cell-substrate interactions and migration in breast cancer. It may serve as a novel predictor of response to endocrine therapy and potential therapeutic target. |
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(1)36  cells |
(17)6 size |
(33)3 lysis |
(49)2 progression, |
| (2)23 suppressor |
(18)6 suppression |
(34)3 onset |
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| (5)19 *null* | (21)5 angiogenesis |
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| (6)17 growth |
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| (7)15 cell |
(23)5 suppressive |
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| (8)14 was |
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(25)4 model |
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(28)3 effects |
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| (13)7 microenvironment |
(29)3 excision |
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| (14)6 formation |
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| (15)6 promotion |
(31)3 had |
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| (16)6 samples |
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--- WordNet output for tumor ---