TGFβ-pathway is down-regulated in a uterine carcinosarcoma: A case study

被引:5
|
作者
Semczuk, Andrzej [1 ]
Zakrzewski, Piotr K. [2 ]
Forma, Ewa [2 ]
Cygankiewicz, Adam I. [2 ]
Semczuk-Sikora, Anna [3 ]
Brys, Magdalena [2 ]
Rechberger, Tomasz [1 ]
Krajewska, Wanda M. [2 ]
机构
[1] Med Univ Lublin, Dept Gynecol 2, Lublin, Poland
[2] Univ Lodz, Fac Biol & Environm Protect, Dept Cytobiochem, PL-90131 Lodz, Poland
[3] Med Univ Lublin, Dept Obstet & Pathol Pregnancy, Lublin, Poland
关键词
TGF beta; Uterine carcinosarcoma; RT-PCR; HUMAN ENDOMETRIAL CANCER; GROWTH-FACTOR; TRANSFORMING GROWTH-FACTOR-BETA-1; II RECEPTORS; EXPRESSION; CARCINOMA; TELOMERASE; HYPOXIA; CARCINOGENESIS; APOPTOSIS;
D O I
10.1016/j.prp.2013.06.017
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
Data assessing the role of various genetic alterations in uterine carcinosarcoma (CS), particularly the transforming growth factors-beta (TGF beta) that play a crucial role in many cellular processes, including proliferation, differentiation, adhesion and migration, are scarce. TGF beta exert their effects through specific receptors and associated auxiliary receptors. In the current study, we investigated the expression of TGF beta isoforms and their receptors, as well as selected genes in a case of CS. We applied the real-time fluorescence detection PCR method with FAM dye-labeled TaqMan specific probes. In a comparison to the normal counterpart, TGFB1, TGFB2, TGFBRII, TGFBR3, ENG and CD109 were all down-regulated in uterine CS samples at different extents. BIRC5 and hTERT, markers of tumor survival, were up-regulated in CS as compared with normal counterparts. A concomitant increase of the hypoxia marker H1F1A expression pattern was noted, whereas the expression of GPR120, responsible for free fatty acids sensing, was not different in both counterparts evaluated. In conclusion, deregulation of various cellular mechanisms in uterine CS is associated with alterations at many levels - cell growth and proliferation, apoptosis, and impaired response to stimuli from extracellular environment. (C) 2013 Elsevier GmbH. All rights reserved.
引用
收藏
页码:740 / 744
页数:5
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