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KIF20A 的过表达通过促进细胞增殖和抑制细胞凋亡赋予肺腺癌恶性表型。

Overexpression of KIF20A confers malignant phenotype of lung adenocarcinoma by promoting cell proliferation and inhibiting apoptosis.

机构信息

The Affiliated Cancer Hospital of Nanjing Medical University, Jiangsu Cancer Hospital, Jiangsu Insititute of Cancer Research, Nanjing, Jiangsu, China.

Department of Oncology, First People's Hospital of Yancheng, Fourth Affliated Hospital of Nantong University, Yancheng, Jiangsu, China.

出版信息

Cancer Med. 2018 Sep;7(9):4678-4689. doi: 10.1002/cam4.1710. Epub 2018 Aug 13.

DOI:10.1002/cam4.1710
PMID:30105795
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6143951/
Abstract

Increasing studies showed that kinesin family member 20A (KIF20A) was overexpessed in several types of cancer, and its overexpression correlated with the oncogenesis and prognosis of cancers. However, little is known about the role of KIF20A in lung adenocarcinoma (LUAD). In this study, we employed the bioinformatics analysis to identify the upregulation of KIF20A in LUAD, then verified the results in human tumor specimens and LUAD cell lines. Compared with normal lung tissues, a ubiquitous upregulation of KIF20A was observed in LUAD tissues by immunohistochemistry (IHC) as well as TCGA analysis. Higher expression of KIF20A was significantly associated with more advanced clinicopathological features and shorter overall survival (OS). Moreover, multivariate Cox regression analysis revealed that KIF20A was an independent prognostic factor for OS. The expression of KIF20A was significantly elevated in LUAD cell lines. After silencing KIF20A, lung cancer cell cycle arrested in G1 phase and apoptosis increased. The same results were observed in vivo. Thus, our study demonstrated that KIF20A might confer malignant phenotype to LUAD by regulating cell proliferation and apoptosis, providing a new potential biomarker for clinical treatment of LUAD.

摘要

越来越多的研究表明，驱动蛋白家族成员 20A（KIF20A）在多种类型的癌症中过表达，其过表达与癌症的发生和预后相关。然而，关于 KIF20A 在肺腺癌（LUAD）中的作用知之甚少。在这项研究中，我们采用生物信息学分析来鉴定 LUAD 中 KIF20A 的上调，然后在人类肿瘤标本和 LUAD 细胞系中验证结果。通过免疫组织化学（IHC）和 TCGA 分析，与正常肺组织相比，LUAD 组织中普遍观察到 KIF20A 的上调。KIF20A 的高表达与更晚期的临床病理特征和更短的总生存期（OS）显著相关。此外，多变量 Cox 回归分析显示 KIF20A 是 OS 的独立预后因素。KIF20A 在 LUAD 细胞系中的表达明显升高。沉默 KIF20A 后，肺癌细胞周期停滞在 G1 期，凋亡增加。在体内也观察到了相同的结果。因此，我们的研究表明，KIF20A 通过调节细胞增殖和凋亡可能赋予 LUAD 恶性表型，为 LUAD 的临床治疗提供了一个新的潜在生物标志物。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/bc029deb2ad4/CAM4-7-4678-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/527a7ac9b1b5/CAM4-7-4678-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/a946a7e787ff/CAM4-7-4678-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/d0f2a62a0846/CAM4-7-4678-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/fcea30bc28f0/CAM4-7-4678-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/bc029deb2ad4/CAM4-7-4678-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/527a7ac9b1b5/CAM4-7-4678-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/9f59c40d9909/CAM4-7-4678-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/a946a7e787ff/CAM4-7-4678-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/d0f2a62a0846/CAM4-7-4678-g004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c5cd/6143951/bc029deb2ad4/CAM4-7-4678-g006.jpg

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