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Retracted :Propofol exerts anticancer activity on hepatocellular carcinoma cells by raising lncRNA DGCR5
Author(s) -
Sun Yan,
Sun Hai
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29202
Subject(s) - hepatocellular carcinoma , wnt signaling pathway , apoptosis , cancer research , viability assay , cell growth , biology , propofol , transfection , cell culture , signal transduction , microbiology and biotechnology , pharmacology , biochemistry , genetics
Hepatocellular carcinoma is one of the most fatal cancers worldwide. Propofol is an intravenous anesthetic extensively used in clinical. Herein, we tested the anticancer activity of propofol on hepatocellular carcinoma, along with the internal molecular mechanism related to lncRNA DiGeorge syndrome critical region gene 5 (DGCR5). Followed by propofol stimulation, hepatocellular carcinoma Huh‐7 and HepG2 cell viability, proliferation, migration, invasion, and apoptosis were tested, respectively. Then, DGCR5 expression levels in hepatocellular carcinoma tissues and cells were measured. sh‐DGCR5 was transfected to silence DGCR5 expression. Subsequently, the influence of DGCR5 silence on propofol caused Huh‐7 and HepG2 cell viability loss, proliferation inhibition, migration and invasion suppression, apoptosis induction, as well as Raf1/ERK1/2 and Wnt/β‐catenin pathways inactivation were assessed, respectively. We discovered that propofol declined Huh‐7 and HepG2 cell viability, proliferation, migration and invasion, but increased cell apoptosis. DGCR5 had a relatively lower expression level in hepatocellular carcinoma tissues and cells. Propofol elevated DGCR5 expression in Huh‐7 and HepG2 cells. Increased expression of DGCR5 was connected with the anticancer activity of propofol on Huh‐7 and HepG2 cells. Besides, propofol repressed Raf1/ERK1/2 and Wnt/β‐catenin pathways through elevating DGCR5 expression. In conclusion, the anticancer activity of propofol on hepatocellular carcinoma was verified in this study. Propofol repressed hepatocellular carcinoma Huh‐7 and HepG2 cell growth and metastasis at least by elevating DGCR5 and hereafter inactivating Raf1/ERK1/2 and Wnt/β‐catenin pathways.