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JAM-A 在非小细胞肺癌中的过表达与肿瘤进展相关。

Overexpression of JAM-A in non-small cell lung cancer correlates with tumor progression.

机构信息

Department of Pathology, First Affiliated Hospital and College of Basic Medical Sciences, China Medical University, Shenyang, People's Republic of China ; Department of Pathology, College of Basic Medical Sciences, Shenyang Medical College, Shenyang, People's Republic of China.

出版信息

PLoS One. 2013 Nov 12;8(11):e79173. doi: 10.1371/journal.pone.0079173. eCollection 2013.

DOI:10.1371/journal.pone.0079173
PMID:24265754
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3827132/
Abstract

The objective of the current study was to determine the clinical significance of junctional adhesion molecule A (JAM-A) in patients with non-small cell lung cancer (NSCLC) and the biological function of JAM-A in NSCLC cell lines. We showed that JAM-A is predominantly expressed in cell membranes and high expression of JAM-A occurred in 37% of lung tumor specimens compared to corresponding normal tissues. High expression of JAM-A was significantly correlated with TNM stage (P = 0.021), lymph node metastasis (P = 0.007), and decreased overall survival (P = 0.02), In addition, we observed that silencing JAM-A by small interfering RNA inhibited tumor cell proliferation and induced cell cycle arrest at the G1/S boundary. Western blotting analysis revealed that knockdown of JAM-A decreased the protein levels of cyclin D1, CDK4, 6, and P-Rb. Thus, JAM-A plays an important role in NSCLC progression.

摘要

本研究旨在探讨细胞间黏附分子 A(JAM-A)在非小细胞肺癌(NSCLC)患者中的临床意义,以及 JAM-A 在 NSCLC 细胞系中的生物学功能。结果表明,JAM-A 主要表达于细胞膜上,与相应的正常组织相比,37%的肺癌组织标本中 JAM-A 呈高表达。JAM-A 的高表达与 TNM 分期(P=0.021)、淋巴结转移(P=0.007)和总生存期缩短显著相关(P=0.02)。此外,我们发现通过小干扰 RNA 沉默 JAM-A 可抑制肿瘤细胞增殖,并诱导细胞周期在 G1/S 期边界停滞。Western blot 分析显示,JAM-A 下调可降低细胞周期蛋白 D1、CDK4、6 和 P-Rb 的蛋白水平。因此,JAM-A 在 NSCLC 的进展中发挥重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/c002b5b3b80d/pone.0079173.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/aee7e38f1a62/pone.0079173.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/75f26b44b755/pone.0079173.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/4d5693c1c836/pone.0079173.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/1e9d8c999cff/pone.0079173.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/e09fd87ba141/pone.0079173.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/3d8f3c318c29/pone.0079173.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/c002b5b3b80d/pone.0079173.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/aee7e38f1a62/pone.0079173.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/75f26b44b755/pone.0079173.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/4d5693c1c836/pone.0079173.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/1e9d8c999cff/pone.0079173.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/e09fd87ba141/pone.0079173.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/3d8f3c318c29/pone.0079173.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6131/3827132/c002b5b3b80d/pone.0079173.g007.jpg

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Oncogene. 2013 May 30;32(22):2799-804. doi: 10.1038/onc.2012.276. Epub 2012 Jul 2.
3
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4
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