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KIFC3 regulates progression of hepatocellular carcinoma via EMT and the AKT/mTOR pathway

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收录情况： ◇ SCIE

作者：
Lu Shimin[1,2] * ; Liu Yinghui[1,2] * ; Tian Shan[3] ; He Yang[1,2] ; Dong Weiguo[1,2,*1] ;
单位： [1]Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China [2]Central Laboratory of Renmin Hospital, Wuhan 430060, Hubei Province, China [3]Department of Infectious Disease, Tongji Hospital Affiliated to Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
出处：
DOI： 10.1016/j.yexcr.2023.113564
ISSN：

关键词： Hepatocellular carcinoma Kinesin AKT/mTOR pathway EMT Inhibitor

摘要：
Hepatocellular carcinoma (HCC) is the fourth leading cause of cancer-related deaths worldwide. Despite an overall downward trend in cancer mortality, HCC-related mortality continues to increase. KIFC3 is involved in cell division and cancers. However, the role of KIFC3 in HCC has yet to be elucidated.A total of 36 cases of HCC tissues, 4 HCC cell lines, and TCGA databases were searched to explore the expression of KIFC3 in HCC. Subsequently, Western blot analysis, immunofluorescence, bioinformatic analysis, molecular docking, and Co-IP were performed to investigate the molecular mechanisms of KIFC3 in HCC.We found that the expression of KIFC3 was upregulated in HCC, and high KIFC3 expression was related to poor overall survival. In addition, the knockdown of KIFC3 inhibited the proliferation, migration, and invasion of HCC cells in vitro, and impeded the growth of HCC in vivo, while overexpression of KIFC3 in HCC cells revealed the opposite effect. Mechanistically, KIFC3 promotes the progression of HCC through the PI3K/AKT/mTOR signalling. And KIFC3 had slight effect on the protein expression of p-PI3K, p-AKT and p-mTOR in TRIP13-ablated or LY294002-treated HCC cells. The KIFC3 knockdown could further enhance the inhibitory effect of LY294002.Our data revealed that KIFC3 is upregulated in HCC and may serve as a novel biomarker for predicting survival in HCC patients. Targeting KIFC3 may serve as a novel therapeutic strategy for HCC patients.Copyright © 2023 Elsevier Inc. All rights reserved.

基金：
National Natural Science Foundation of China, No.81870392.
语种：
外文
被引次数：
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中科院(CAS)分区：
出版当年[2022]版：
大类 | 3 区 医学
小类 | 4 区 肿瘤学 4 区 细胞生物学
最新[2025]版：
大类 | 3 区 生物学
小类 | 4 区 细胞生物学 4 区 肿瘤学
JCR分区：
出版当年[2021]版：
Q3 CELL BIOLOGY Q3 ONCOLOGY
最新[2023]版：
Q2 ONCOLOGY Q3 CELL BIOLOGY

影响因子： 最新[2023版] 最新五年平均 出版当年[2021版] 出版当年五年平均 出版前一年[2020版] 出版后一年[2022版]

第一作者：
第一作者单位： [1]Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China [2]Central Laboratory of Renmin Hospital, Wuhan 430060, Hubei Province, China
共同第一作者：
通讯作者：
通讯机构： [1]Department of Gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China [2]Central Laboratory of Renmin Hospital, Wuhan 430060, Hubei Province, China [*1]Department of gastroenterology, Renmin Hospital of Wuhan University, Wuhan 430060, Hubei Province, China
推荐引用方式(GB/T 7714)：
Lu Shimin,Liu Yinghui,Tian Shan,et al.KIFC3 regulates progression of hepatocellular carcinoma via EMT and the AKT/mTOR pathway[J].EXPERIMENTAL CELL RESEARCH.2023,426(1):doi:10.1016/j.yexcr.2023.113564.
APA：
Lu Shimin,Liu Yinghui,Tian Shan,He Yang&Dong Weiguo.(2023).KIFC3 regulates progression of hepatocellular carcinoma via EMT and the AKT/mTOR pathway.EXPERIMENTAL CELL RESEARCH,426,(1)
MLA：
Lu Shimin,et al."KIFC3 regulates progression of hepatocellular carcinoma via EMT and the AKT/mTOR pathway".EXPERIMENTAL CELL RESEARCH 426..1(2023)

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