کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8524945 | 1557936 | 2018 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Conditioned medium from stimulated macrophages inhibits growth but induces an inflammatory phenotype in breast cancer cells
ترجمه فارسی عنوان
محیط تهیه شده از ماکروفاژهای تحریک شده مانع از رشد و پیشرفت فنوتیپ التهابی در سلولهای سرطانی پستان می شود
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کلمات کلیدی
PCNAGLB1CDKN1Aphorbol 12-myristate 13-acetateIL-6IL-8Bcl-2qRT-PCRDMSO - DMSOPMA - LDC هاMTT - MTTProliferating Cell Nuclear Antigen - آنتیژن هسته ای تکثیر سلولیAutophagy - اتوفاژیinflammation - التهاب( توروم) interleukin 6 - اینترلوکین 6Interleukin 8 - اینترلوکین 8TAM - تامTumor associated macrophage - تومور مرتبط با ماکروفاژtumor necrosis factor- alpha - تومور نکروز فاکتور آلفاApoptosis - خزان یاختهایDimethyl sulfoxide - دیمتیل سولفواکسیدBreast cancer - سرطان پستانTNF-α - فاکتور نکروز توموری آلفاB-cell lymphoma-2 - لنفوم سلول B-2Macrophage - ماکروفاژ cyclin-dependent kinase inhibitor 1A - مهار کننده 1A کیناز وابسته به کینازquantitative real-time polymerase chain reaction - واکنش زنجیره ای پلیمراز کمی زمان واقعی استSenescence - پیری
موضوعات مرتبط
علوم پزشکی و سلامت
پزشکی و دندانپزشکی
تومور شناسی
چکیده انگلیسی
Disparate roles exist for tumor-associated macrophages in breast cancer growth and progression. The aim of this study was to explore the influence of induced macrophages on the growth of breast cancer cells. THP-1 monocytes were differentiated to macrophages using phorbol 12-myristate 13-acetate. The effect of the medium from THP-1 monocytes or macrophage-conditioned medium (MÏCM) on MCF-7 (estrogen receptor and progesterone-positive positive) and MDA-MB-231 (MB; triple-negative) breast cancer cells was determined at 24â¯h, 48â¯h and 72â¯h. Assays were conducted for cell viability, apoptosis, proliferation and cell phenotype, and quantitative real-time polymerase chain reaction (qRT-PCR) for expression of associated genes. MÏCM inhibited proliferation of MCF-7 and MB cells in a time-dependent manner and, in particular, decreased viability of MCF-7 cells. MÏCM induced a markedly vacuolated phenotype in MCF-7 increased apoptosis in MCF-7 cells, but correlative changes in Bcl-2 or Bax were absent. A multifold and significant reduction in anti-apoptotic Bcl-2 in MB cells was not matched by increased apoptosis. The cell cycle inhibitor CDKN1A was increased in both cell lines, but PCNA decreased only in MB cells. Senescence-associated galactosidase beta-1 (GLB1) mRNA was decreased in MCF-7 cells (48 and 72â¯h) but increased in MB cells (72â¯h). Increased expression of interleukin-6 (IL-6) and IL-8 was seen in both cell lines, and increased tumor necrosis factor- α was seen at 24â¯h for MB and 72â¯h for MCF-7 indicating increased inflammatory responses of the cancer cells. The two breast cancer celllines had different responses to MÏCM, mainly involving inhibition rather than stimulation of growth of the cells, stimulation of senescence (MB cells) and increased inflammatory cytokine expression. The estrogen and progesterone receptor status of the cell lines may determine their response to MÏCM. The function of the inflammatory cytokines in breast cancer growth remains to be identified.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Biomedicine & Pharmacotherapy - Volume 106, October 2018, Pages 247-254
Journal: Biomedicine & Pharmacotherapy - Volume 106, October 2018, Pages 247-254
نویسندگان
Wenzhe Song, Parth Thakor, David A. Vesey, Glenda C. Gobe, Christudas Morais,