中文版 | English
Title

KIF22 Promotes Development of Pancreatic Cancer by Regulating the MEK/ERK/P21 Signaling Axis

Author
Publication Years
2022
DOI
Source Title
ISSN
2314-6133
EISSN
2314-6141
Volume2022
Abstract
The study is aimed at exploring the potential biological process and molecular mechanism of KIF22 involved in the development and progression of pancreatic cancer. First, we used the GEPIA database and tissue qRT-PCR to examine the expression of KIF22 mRNA in pancreatic cancer. Meanwhile, immunohistochemistry revealed the presence of KIF22 in 71 pancreatic cancer tissues versus 30 paracarcinoma tissues. Then, we also explored the relationship between KIF22 expression level and clinical prognosis. Furthermore, in pancreatic cancer cells, we silenced KIF22 by transfecting KIF22 SiRNA, and we investigated the effect of KIF22 on the proliferation of pancreatic cancer cells with MTT and colony formation assays. Finally, we used Gene Set Enrichment Analysis (GSEA) to look at the effect of KIF22 on the cell cycle regulation of pancreatic cancer cells, and we used Western blot to look at the relationship between KIF22 and the phosphorylated MEK1/2, ERK1/2 (p-MEK1/2, p-ERK1/2), and the cyclin-dependent kinase inhibitor (P21). In this study, we found that KIF22 was highly expressed in pancreatic cancer tissues, and patients with high expression of KIF22 demonstrated significantly worse clinical prognosis outcomes (P<0.05). When the KIF22 gene was silenced in pancreatic cancer cells (PANC-1 and MIA PaCa-2), the cells' ability to proliferate was significantly reduced. Furthermore, GSEA confirmed that KIF22 is involved in cell cycle regulation in pancreatic cancer patients (FDR=0.00158, P<0.0001). Besides, the level of KIF22 expression was positively correlated with Ki67 (r=0.8043, P<0.0001), and KIF22 can promote the transmutation of G1/S. The expression of p-MEK1/2 and p-ERK1/2 was significantly downregulated, while P21 expression was significantly upregulated (P<0.05). According to our findings, KIF22 is highly expressed in pancreatic cancer and demonstrates a poor clinical prognosis. It regulates the cell cycle via the MEK/ERK/P21 signaling axis and promotes the development of pancreatic cancer.
URL[Source Record]
Indexed By
Language
English
SUSTech Authorship
First
WOS Accession No
WOS:000802855900006
Scopus EID
2-s2.0-85130366135
Data Source
Scopus
Citation statistics
Cited Times [WOS]:2
Document TypeJournal Article
Identifierhttp://kc.sustech.edu.cn/handle/2SGJ60CL/411948
DepartmentSouthern University of Science and Technology Hospital
Affiliation
1.Southern University of Science and Technology Hospital,Shenzhen,No. 6019, Liuxian Avenue, Nanshan District, Guangdong,China
2.Gansu Provincial Hospital,Gansu,No. 204, Donggang West Road, Chengguan District, Lanzhou,China
3.Lanzhou University Second Hospital,Gansu,No. 82, Cuiyingmen, Chengguan District, Lanzhou,China
First Author AffilicationSouthern University of Science and Technology Hospital
First Author's First AffilicationSouthern University of Science and Technology Hospital
Recommended Citation
GB/T 7714
Zhang,Ruiyun,Ma,Li,Wei,Yucai,et al. KIF22 Promotes Development of Pancreatic Cancer by Regulating the MEK/ERK/P21 Signaling Axis[J]. Biomed Research International,2022,2022.
APA
Zhang,Ruiyun.,Ma,Li.,Wei,Yucai.,Wei,Kongkong.,Song,Tianliang.,...&Feng,Zhijun.(2022).KIF22 Promotes Development of Pancreatic Cancer by Regulating the MEK/ERK/P21 Signaling Axis.Biomed Research International,2022.
MLA
Zhang,Ruiyun,et al."KIF22 Promotes Development of Pancreatic Cancer by Regulating the MEK/ERK/P21 Signaling Axis".Biomed Research International 2022(2022).
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