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Overexpression of 15-Hydroxyprostaglandin Dehydrogenase Inhibits A549 Lung Adenocarcinoma Cell Growth via Inducing Cell Cycle Arrest and Inhibiting Epithelial-Mesenchymal Transition
Author(s) -
Weixuan Wang,
Changmei Yang,
Haiteng Deng
Publication year - 2021
Publication title -
cancer management and research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.024
H-Index - 40
ISSN - 1179-1322
DOI - 10.2147/cmar.s331222
Subject(s) - a549 cell , cell growth , cancer research , adenocarcinoma , cell cycle , epithelial–mesenchymal transition , pi3k/akt/mtor pathway , cell cycle checkpoint , protein kinase b , cell , biology , apoptosis , lung cancer , chemistry , downregulation and upregulation , cancer , microbiology and biotechnology , signal transduction , pathology , medicine , biochemistry , gene , genetics
Lung cancer is one of the most commonly diagnosed cancer as well as the leading cause of cancer-related mortality worldwide, among which lung adenocarcinoma (LUAD) is the most frequent form of lung cancer. Previous studies have shown that 15-hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes the oxidation of prostaglandins to reduce their biological activities and behaves as a tumor suppressor in various cancers. Thus, we aimed to systematically examine the effects of 15-PGDH overexpression on cellular processes in lung adenocarcinoma cells.

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