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POTEE stimulates the proliferation of pancreatic cancer by activating the PI3K /Akt/ GSK ‐3β/β‐catenin signaling
Author(s) -
Hao Qingya,
Gao Lihua,
Niu Wenyang,
Chen Liang,
Zhang Peng,
Chen Zhong
Publication year - 2020
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1640
Subject(s) - pancreatic cancer , protein kinase b , pi3k/akt/mtor pathway , gene knockdown , cancer research , cancer , medicine , downregulation and upregulation , ca19 9 , catenin , signal transduction , chemistry , biology , wnt signaling pathway , apoptosis , microbiology and biotechnology , gene , biochemistry
To explore the role of POTEE in the malignant development of pancreatic cancer and the possible mechanism. POTEE levels in pancreatic cancer samples were detected. The relationship between POTEE level and clinical data of pancreatic cancer patients was analyzed. After knockdown of POTEE or treatment of the GSK‐3β inhibitor, proliferative change in pancreatic cancer cells was assessed. Protein levels of vital genes in the PI3K/Akt/GSK‐3β/β‐catenin signaling influenced by POTEE were examined. POTEE was upregulated in pancreatic cancer samples. High level of POTEE indicated advanced tumor staging, large tumor size, and poor prognosis in pancreatic cancer patients. Knockdown of POTEE or treatment of Tideglusib remarkably attenuated proliferative ability in pancreatic cancer cells. Vital genes in the PI3K/Akt/GSK‐3β/β‐catenin signaling were downregulated by knockdown of POTEE. POTEE stimulates the proliferative ability in pancreatic cancer by activating the PI3K/Akt/GSK‐3β/β‐catenin signaling. High level of POTEE indicates advanced tumor staging, large tumor size and poor prognosis in pancreatic cancer patients.