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学科主题: 临床医学
题名:
Tumorigenesis of K-ras mutation in human endometrial carcinoma via upregulation of estrogen receptor
作者: 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
发表日期: 2006-05-01
DOI: 10.1016/j.ygyno.2005.10.016
卷: 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
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/57181
Appears in Collections:北京大学第二临床医学院_妇科_期刊论文

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作者单位: Peking Univ, Peoples Hosp, Dept Gynecol, Beijing 100044, Peoples R China

Recommended Citation:
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.
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