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骨巨细胞瘤患者中程序性细胞死亡4表达降低的临床意义

Clinical significance of decreased programmed cell death 4 expression in patients with giant cell tumors of the bone.

作者信息

Gao Fei, Zhang Wei, Ding Lingling, Zhao Miaoqing, Ma Zhe, Huang Shanying

机构信息

The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Shandong University Qilu Hospital, Jinan, Shandong 250012, P.R. China.

Department of Orthopedics, Shandong Provincial Hospital Affiliated to Shandong University, Jinan, Shandong 250021, P.R. China.

出版信息

Oncol Lett. 2018 Sep;16(3):3805-3811. doi: 10.3892/ol.2018.9087. Epub 2018 Jul 5.

DOI:10.3892/ol.2018.9087
PMID:30127992
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6096107/
Abstract

Programmed cell death 4 (PDCD4) has been recognized as a novel tumor suppressor gene, which inhibits the activation and translation of activator protein (AP)-1. Dysregulated expression of PDCD4 is also involved in various human tumors and is linked to tumor progression and development. However, the function and clinical implication of PDCD4 in giant cell tumors of the bone (GCTBs) has not been previously investigated. In the present study, PDCD4 expression was determined in 83 samples of GCTBs at mRNA and protein levels by quantitative reverse transcription-polymerase chain reaction, western blotting and immunohistochemistry. The results demonstrated that PDCD4 mRNA expression was reduced in 63% of GCTB samples (17/27) and protein expression was decreased in 65% of samples (54/83), compared with adjacent non-tumor tissues. Furthermore, decreased expression of PDCD4 was significantly associated with certain clinicopathological characteristics, including the Campanacci grade and recurrence. A strong negative correlation was determined between PDCD4 expression and the Ki-67 positive rate in GCTBs (r=-0.6392; P<0.001). The results of the present study suggest that PDCD4 may serve a role in the malignant progression of human GCTBs and may be an important prediction factor for prognosis.

摘要

程序性细胞死亡4(PDCD4)已被公认为一种新型肿瘤抑制基因,它可抑制激活蛋白(AP)-1的激活和翻译。PDCD4表达失调也与多种人类肿瘤有关,并与肿瘤的进展和发展相关。然而,PDCD4在骨巨细胞瘤(GCTB)中的功能和临床意义此前尚未得到研究。在本研究中,通过定量逆转录-聚合酶链反应、蛋白质印迹法和免疫组织化学在mRNA和蛋白质水平上测定了83例GCTB样本中的PDCD4表达。结果表明,与相邻的非肿瘤组织相比,63%的GCTB样本(17/27)中PDCD4 mRNA表达降低,65%的样本(54/83)中蛋白质表达下降。此外,PDCD4表达降低与某些临床病理特征显著相关,包括坎帕纳奇分级和复发。在GCTB中,PDCD4表达与Ki-67阳性率之间存在强烈的负相关(r=-0.6392;P<0.001)。本研究结果表明,PDCD4可能在人类GCTB的恶性进展中起作用,并且可能是预后的重要预测因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/a8c0cc7554f1/ol-16-03-3805-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/cb72981f409e/ol-16-03-3805-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/883adde99b57/ol-16-03-3805-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/4277dd35ba84/ol-16-03-3805-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/c0320b3f1dd1/ol-16-03-3805-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/eae807d111bd/ol-16-03-3805-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/a8c0cc7554f1/ol-16-03-3805-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/cb72981f409e/ol-16-03-3805-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/883adde99b57/ol-16-03-3805-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/4277dd35ba84/ol-16-03-3805-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/c0320b3f1dd1/ol-16-03-3805-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/eae807d111bd/ol-16-03-3805-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5fa1/6096107/a8c0cc7554f1/ol-16-03-3805-g05.jpg

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MicroRNA-150 promotes cell proliferation, migration, and invasion of cervical cancer through targeting PDCD4.微小 RNA-150 通过靶向 PDCD4 促进宫颈癌的细胞增殖、迁移和侵袭。
Biomed Pharmacother. 2018 Jan;97:511-517. doi: 10.1016/j.biopha.2017.09.143. Epub 2017 Nov 6.
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miR-23a/b promote tumor growth and suppress apoptosis by targeting PDCD4 in gastric cancer.
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Cell Death Dis. 2017 Oct 5;8(10):e3059. doi: 10.1038/cddis.2017.447.
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The miR-93 promotes proliferation by directly targeting PDCD4 in hepatocellular carcinoma.miR-93 通过直接靶向 PDCD4 促进肝癌细胞增殖。
Neoplasma. 2017;64(5):770-777. doi: 10.4149/neo_2017_516.
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Giant cell tumour of bone in the denosumab era.地诺单抗时代的骨巨细胞瘤
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