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肝脏、肝细胞及肝癌细胞系中p16表达水平的差异

Differential p16 expression levels in the liver, hepatocytes and hepatocellular cell lines.

作者信息

Kramar Barbara, Šuput Dušan, Milisav Irina

机构信息

University of Ljubljana, Faculty of Medicine, Institute of Pathophysiology, Zaloska 4, Ljubljana, Slovenia.

University of Ljubljana, Laboratory of oxidative stress research, Faculty of Health Sciences, Zdravstvena pot 5, Ljubljana, Slovenia.

出版信息

PeerJ. 2021 Nov 2;9:e12358. doi: 10.7717/peerj.12358. eCollection 2021.

DOI:10.7717/peerj.12358
PMID:34760375
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8570159/
Abstract

BACKGROUND

One of the most frequently deleted genes in cancer is encoding p16. This protein is often overexpressed in senescent cells, while its suppression can bypass the oncogene-induced senescence to enable transformation and tumorigenesis. The roles of the protein p16 are recently being expanded from the cell cycle progression regulator to the cellular regulator interacting in several different pathways. Yet data on its liver and liver cells' expression are inconclusive.

METHODS

The expression of the gene in liver and liver cells was determined by RT-qPCR and compared to its protein amounts by western blotting.

RESULTS

is expressed at low levels in the liver and rat hepatocytes. Its expression varies from none to the considerable levels in the examined hepatocellular carcinoma cell lines (FaO and HepG2) and in immortalized mouse hepatocytes. Such significant expression differences of an important cellular regulator warrant the need to closely examine the differences in biochemical pathways correlated with the expression when using hepatocytes and hepatoma liver models.

摘要

背景

癌症中最常被删除的基因之一是编码p16的基因。这种蛋白质在衰老细胞中常过度表达,而对其抑制可绕过癌基因诱导的衰老,从而实现细胞转化和肿瘤发生。蛋白质p16的作用最近正从细胞周期进程调节因子扩展到在多种不同途径中相互作用的细胞调节因子。然而,关于其在肝脏和肝细胞中的表达数据尚无定论。

方法

通过逆转录定量聚合酶链反应(RT-qPCR)测定该基因在肝脏和肝细胞中的表达,并通过蛋白质印迹法将其与蛋白质含量进行比较。

结果

该基因在肝脏和大鼠肝细胞中低水平表达。在所检测的肝癌细胞系(FaO和HepG2)以及永生化小鼠肝细胞中,其表达水平从无到相当高不等。这种重要细胞调节因子的显著表达差异,使得在使用肝细胞和肝癌肝脏模型时,有必要密切研究与该基因表达相关的生化途径差异。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f9b/8570159/eae4e81fbc2b/peerj-09-12358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f9b/8570159/aeddd99c0ef2/peerj-09-12358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f9b/8570159/decd8b88afd6/peerj-09-12358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f9b/8570159/eae4e81fbc2b/peerj-09-12358-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f9b/8570159/aeddd99c0ef2/peerj-09-12358-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f9b/8570159/decd8b88afd6/peerj-09-12358-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6f9b/8570159/eae4e81fbc2b/peerj-09-12358-g003.jpg

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