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有丝分裂着丝粒相关驱动蛋白在人胃癌中过表达的临床病理及生物学意义

Clinicopathological and biological significance of mitotic centromere-associated kinesin overexpression in human gastric cancer.

作者信息

Nakamura Y, Tanaka F, Haraguchi N, Mimori K, Matsumoto T, Inoue H, Yanaga K, Mori M

机构信息

Department of Surgery and Molecular Oncology, Medical Institute of Bioregulation, Kyushu University, 4546 Tsurumibaru, Beppu 874-0838, Japan.

出版信息

Br J Cancer. 2007 Aug 20;97(4):543-9. doi: 10.1038/sj.bjc.6603905. Epub 2007 Jul 24.

Abstract

Mitotic centromere-associated kinesin (MCAK) is a microtubule (MT) depolymerase necessary for ensuring proper kinetochore MT attachment during spindle formation. To determine MCAK expression status and its clinicopathological significance, real-time reverse transcriptase-polymerase chain reaction was used in 65 cases of gastric cancer. MCAK gene expression in cancer tissue was significantly higher than expression in non-malignant tissue (P<0.05). Elevated MCAK expression was significantly associated with lymphatic invasion (P=0.01) and lymph node metastasis (P=0.04). Furthermore, patients with high MCAK expression had a significantly poorer survival rate than those with low MCAK expression (P=0.008). Immunohistochemical study revealed that expression of MCAK was primarily observed in cancer cells. Additionally, a gastric cancer cell line (AZ521) that stably expressed MCAK was established and used to investigate the biological effects of the MCAK gene. In vitro results showed that cells transfected with MCAK had a high rate of proliferation (P<0.001) and increased migratory ability (P<0.001) compared to mock-transfected cells. This study demonstrated that elevated expression of MCAK may be associated with lymphatic invasion, lymph node metastasis, and poor prognosis. These characteristics may be due in part to the increased proliferative and migratory ability of cells expressing MCAK.

摘要

有丝分裂着丝粒相关驱动蛋白(MCAK)是一种微管(MT)解聚酶,对于在纺锤体形成过程中确保着丝粒微管正确附着是必需的。为了确定MCAK的表达状态及其临床病理意义,对65例胃癌患者进行了实时逆转录聚合酶链反应。癌组织中MCAK基因表达显著高于非癌组织(P<0.05)。MCAK表达升高与淋巴侵犯(P=0.01)和淋巴结转移(P=0.04)显著相关。此外,MCAK高表达患者的生存率显著低于MCAK低表达患者(P=0.008)。免疫组织化学研究显示,MCAK表达主要见于癌细胞。另外,建立了稳定表达MCAK的胃癌细胞系(AZ521),并用于研究MCAK基因的生物学效应。体外实验结果显示,与mock转染细胞相比,转染MCAK的细胞增殖率较高(P<0.001),迁移能力增强(P<0.001)。本研究表明,MCAK表达升高可能与淋巴侵犯、淋巴结转移及预后不良有关。这些特征可能部分归因于表达MCAK的细胞增殖和迁移能力增强。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bee6/2360338/b70a60ac7768/6603905f1.jpg

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