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Tumorigenesis of K-ras mutation in human endometrial carcinoma via upregulation of estrogen receptor
Tu, Z; Gui, LM; Wang, JL; Li, XP; Sun, PM; Wei, LH
关键词Endometrial Carcinoma K-ras Estrogen Receptor Signaling Pathway Tumorigenesis
刊名GYNECOLOGIC ONCOLOGY
2006-05-01
DOI10.1016/j.ygyno.2005.10.016
101期:2页:274-279
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Oncology ; Obstetrics & Gynecology
研究领域[WOS]Oncology ; Obstetrics & Gynecology
关键词[WOS]MOLECULAR-GENETIC-PATHWAYS ; POINT MUTATIONS ; H-RAS ; CANCER ; P53 ; CELLS ; ACTIVATION ; ADENOCARCINOMAS ; TRANSFORMATION ; EXPRESSION
英文摘要

Objective. To investigate the tumorigenesis of mutant [(12)Asp]-K-ras in endometrial carcinoma and its relationship with ER.

Methods. We constructed pcDl-[(12)Asp]K-ras4B by inserting full-length [(12)Asp]K-ras4B from human endometrial carcinoma Hec-1A cells, into pcDI vector. Cell proliferation of NIH3T3 after transfection with pcDI-[(12)Asp]K-ras4B was measured by MTT assay. The cell transformation was determined by colony formation and tumor nodule development. [(12)Asp]-K-ras4B-NIH3T3 cells were transfected with constitutively active pCMV-RafCAAX and dominant-negative pCMV-RafS621 A. Cell growth was measured by MTT assay and [3 H]thymidine incorporation. After transfected with pcDl-[(12)Asp]K-ras4B or pCMV-RafS621A, the cells were harvested for Western blot and reporter assay to determine the expression and transcriptional activity of ERu. and ER, respectively.

Results. [(12)Asp]-K-ras4B enhanced NIH3T3 cells proliferation after 48 h post-transfection (P < 0.05). More colonies were grown 10 days after incubating pcDI-[(12)Asp]-K-ras4B-NIH3T3 cells (13.48%) than pcDI-NIH3T3 (4.26%) or untreated NIH3T3 (2.33%). The pcDI-[(12)Asp]-Kras4B-NIH3T3 cells injected to the nude mice Balb/C developed tumor nodules with poor-differentiated cells after 12 days. An increase of ER alpha and ER was observed in pcDI-[(12)Asp]-K-ras4B-NIH3T3 cells. RafS621A downregulated ER alpha and ER beta expression. Estrogen induced the ER transcriptional activity by 5-fold in pcDI-NIH3T3 cells, 13-fold in pcDI-[(12)Asp]K-ras4B-NIH3T3 and 19-fold in HEC-IA. RafS621A suppressed the ER transcriptional activity.

Conclusions. K-ras mutation induces tumorigenesis in endometrium, and this malignant transformation involves Raf signaling pathway and ER. (c) 2005 Elsevier Inc. All rights reserved.

语种英语
WOS记录号WOS:000237813700017
引用统计
被引频次:14[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/57181
专题北京大学第二临床医学院_妇科
作者单位Peking Univ, Peoples Hosp, Dept Gynecol, Beijing 100044, Peoples R China
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Tu, Z,Gui, LM,Wang, JL,et al. Tumorigenesis of K-ras mutation in human endometrial carcinoma via upregulation of estrogen receptor[J]. GYNECOLOGIC ONCOLOGY,2006,101(2):274-279.
APA Tu, Z,Gui, LM,Wang, JL,Li, XP,Sun, PM,&Wei, LH.(2006).Tumorigenesis of K-ras mutation in human endometrial carcinoma via upregulation of estrogen receptor.GYNECOLOGIC ONCOLOGY,101(2),274-279.
MLA Tu, Z,et al."Tumorigenesis of K-ras mutation in human endometrial carcinoma via upregulation of estrogen receptor".GYNECOLOGIC ONCOLOGY 101.2(2006):274-279.
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