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BUB1通过激活SMAD2磷酸化促进肝癌细胞增殖。

BUB1 promotes proliferation of liver cancer cells by activating SMAD2 phosphorylation.

作者信息

Zhu Li-Jing, Pan Yan, Chen Xiao-Ying, Hou Pan-Fei

机构信息

Department of Radiation Oncology, Lianshui County People's Hospital, Huaian, Jiangsu 223400, P.R. China.

Department of Clinical Laboratory, Lianshui County People's Hospital, Huaian, Jiangsu 223400, P.R. China.

出版信息

Oncol Lett. 2020 May;19(5):3506-3512. doi: 10.3892/ol.2020.11445. Epub 2020 Mar 5.

DOI:10.3892/ol.2020.11445
PMID:32269624
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7114935/
Abstract

Budding uninhibited by benzimidazoles 1 (BUB1) is a mitotic checkpoint serine/threonine kinase that has been reported as an oncogene or tumor suppressor gene in various types of cancer, including breast cancer, pancreatic ductal adenocarcinoma, prostate and gastric cancers. However, its role in liver cancer remains unclear. The present study aimed to explore the biological function of BUB1 in liver cancer. The present study demonstrated that BUB1 mRNA expression levels and the intensity of immunohistochemical staining were significantly increased in liver cancer tissues compared with normal tissues. The role of BUB1 in cell proliferation was also determined. Overexpression of BUB1 significantly promoted cell proliferation, whereas knockdown of BUB1 expression inhibited the proliferation of liver cancer cell lines. In experiments investigating the underlying mechanism, overexpression of BUB1 increased the levels of SMAD2 phosphorylation, whereas knockdown of BUB1 reduced the levels of SMAD2 phosphorylation. Therefore, BUB1 may promote proliferation of liver cancer cells by activating phosphorylation of SMAD2, and BUB1 may serve as a potential target in the diagnosis and/or treatment of liver cancer.

摘要

苯并咪唑不抑制的芽殖蛋白1(BUB1)是一种有丝分裂检查点丝氨酸/苏氨酸激酶,在包括乳腺癌、胰腺导管腺癌、前列腺癌和胃癌在内的多种癌症中,它被报道为癌基因或肿瘤抑制基因。然而,其在肝癌中的作用仍不清楚。本研究旨在探讨BUB1在肝癌中的生物学功能。本研究表明,与正常组织相比,肝癌组织中BUB1 mRNA表达水平和免疫组化染色强度显著增加。还确定了BUB1在细胞增殖中的作用。BUB1的过表达显著促进细胞增殖,而BUB1表达的敲低则抑制肝癌细胞系的增殖。在研究潜在机制的实验中,BUB1的过表达增加了SMAD2磷酸化水平,而BUB1的敲低则降低了SMAD2磷酸化水平。因此,BUB1可能通过激活SMAD2磷酸化来促进肝癌细胞增殖,并且BUB1可能作为肝癌诊断和/或治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/09f167274604/ol-19-05-3506-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/e84792a28baf/ol-19-05-3506-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/6642fc3495da/ol-19-05-3506-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/6fd8a2fbbad2/ol-19-05-3506-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/5442c7954290/ol-19-05-3506-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/09f167274604/ol-19-05-3506-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/e84792a28baf/ol-19-05-3506-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/6642fc3495da/ol-19-05-3506-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/6fd8a2fbbad2/ol-19-05-3506-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/5442c7954290/ol-19-05-3506-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c018/7114935/09f167274604/ol-19-05-3506-g04.jpg

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