L-Tetrahydropalmatine Inhibits the Progression of Glioblastoma Tumor by Suppressing the Extracellular-Signal-Regulated Kinase/Nuclear Factor-Kappa B Signaling Pathway.

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Authors: Feng Xue and Tingting Chen
Date: May 2021
Publisher: New Century Health Publishers, LLC
Document Type: Article
Length: 3,953 words
Lexile Measure: 1380L

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Abstract :

Glioblastoma multiforme is the most common malignancy of central nervous system. Herein we have evaluated the effect of L-tetrahydropalmatine, an isoquinoline alkaloid, on the tumor growth both in vivo and in vitro using C6 glioblastoma multiforme cells and BALB/c mice injected subcutaneously with C6/luc2 cells. The results of these studies show that L-tetrahydropalmatine exhibited cytotoxic effect on C6 glioblastoma multiforme cells, suppressed nuclear factor-kappa B activity, suppressed the levels of tumor-linked proteins such as matrix metalloproteinase-2/9, Cyclin-D1, vascular endothelial growth factor, and X-linked inhibitor of apoptosis protein via ERK/nuclear factor-kappa B cascade. Further, L-tetrahydropalmatine inhibited the cell migration and invasion properties of C6 cells, and also suppressed the tumor weight and volume in mice. Immunohistochemical staining of tumor tissues suggested that L-tetrahydropalmatine inhibited the extracellular-signal-regulated kinase/nuclear factor-kappa B cascade and suppressed the levels of Cyclin-D1; matrix metalloproteinase-2/9; X-linked inhibitor of apoptosis protein; and vascular endothelial growth factor, and also the progression and growth of glioblastoma multiforme in mice. In summary, L-tetrahydropalmatine inhibits the ERK/nuclear factor-kappa B cascade, decreases the tumor volume, and inhibits the proteins responsible for tumor growth both in vivo and in vitro. Keywords: C6 cells, ERK/NF-[kappa]B, Glioblastoma, L-THP Abbreviations Used: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide, MTT; Central nervous system, CNS; Dimethyl sulfoxide, DMSO; Epidermal growth factor receptor, EGFR; Extracellular-signal-regulated kinase, ERK; Glioblastoma multiforme, GBM; Hematoxylin and Eosin, H&E; Immunohistochemistry, IHC; L-tatrahydropalmatine, L-THP; Matrix metalloproteinase, MMP; Mitogen-activated protein kinase, MEK; Mitogen-activated protein kinase, MAPK; Nonsteroidal anti-inflammatory drugs, NSAIDS; Nuclear factor-kappa B, NFkB; Phosphate-buffered saline, PBS; Phosphoinositide 3-kinase, PI3K; Phosphorylated-extracellularsignal-regulated kinase, pERK; Platelet-derived growth factor receptor, PDGFR; Protein kinase B, AKT; The extracellular-signalregulated kinase/Nuclear factor-kappa B, ERK/NF-[kappa]B; Vascular endothelial growth factor receptor, VEGFR; Vascular endothelial growth factor, VEGF; X-linked inhibitor of apoptosis protein, XIAP Corresponding Author: Dr. Tingting Chen, Department of Neurosurgery, Tianjin Hospital of ITCWM Nan Kai Hospital, Tianjin, China; E-mail: wind88566@163.com

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Gale Document Number: GALE|A659273148