Please use this identifier to cite or link to this item: https://doi.org/10.18632/oncotarget.3443
Title: Brassinin inhibits STAT3 signaling pathway through modulation of PIAS-3 and SOCS-3 expression and sensitizes human lung cancer xenograft in nude mice to paclitaxel
Authors: Lee, J.H
Kim, C
Sethi, G 
Ahn, K.S
Keywords: brassinin
CD31 antigen
interleukin 6
Ki 67 antigen
paclitaxel
phytoalexin
PIAS 3
protein inhibitor of activated STAT
small interfering RNA
STAT3 protein
suppressor of cytokine signaling 3
unclassified drug
brassinin
chaperone
indole derivative
paclitaxel
PIAS3 protein, human
protein inhibitor of activated STAT
SOCS3 protein, human
STAT3 protein
STAT3 protein, human
suppressor of cytokine signaling
suppressor of cytokine signaling 3
thiocarbamic acid derivative
animal experiment
animal model
animal tissue
apoptosis
Article
cancer cell
carcinogenesis
cell invasion
cell proliferation
cell viability
controlled study
down regulation
drug cytotoxicity
drug sensitization
drug structure
female
gene induction
gene product
gene silencing
human
human cell
mouse
mouse model
non small cell lung cancer
nonhuman
nude mouse
protein expression
protein induction
protein phosphorylation
signal transduction
tumor growth
tumor xenograft
animal
antagonists and inhibitors
drug effects
drug screening
genetic transfection
K-562 cell line
male
metabolism
randomization
signal transduction
tumor cell line
Animals
Cell Line, Tumor
Cell Proliferation
Humans
Indoles
K562 Cells
Male
Mice
Mice, Nude
Molecular Chaperones
Paclitaxel
Protein Inhibitors of Activated STAT
Random Allocation
Signal Transduction
STAT3 Transcription Factor
Suppressor of Cytokine Signaling 3 Protein
Suppressor of Cytokine Signaling Proteins
Thiocarbamates
Transfection
Xenograft Model Antitumor Assays
Issue Date: 2015
Publisher: Impact Journals LLC
Citation: Lee, J.H, Kim, C, Sethi, G, Ahn, K.S (2015). Brassinin inhibits STAT3 signaling pathway through modulation of PIAS-3 and SOCS-3 expression and sensitizes human lung cancer xenograft in nude mice to paclitaxel. Oncotarget 6 (8) : 6386-6405. ScholarBank@NUS Repository. https://doi.org/10.18632/oncotarget.3443
Rights: Attribution 4.0 International
Abstract: Persistent phosphorylation of signal transducers and activators of transcription 3 (STAT3) is frequently observed in tumor cells. We found that brassinin (BSN) suppressed both constitutive and IL-6-inducible STAT3 activation in lung cancer cells. Moreover, BSN induced PIAS-3 protein and mRNA, whereas the expression of SOCS-3 was reduced. Knockdown of PIAS-3 by small interfering RNA prevented inhibition of STAT3 and cytotoxicity by BSN. Overexpression of SOCS-3 in BSNtreated cells increased STAT3 phosphorylation and cell viability. BSN down-regulated STAT3-regulated gene products, inhibited proliferation, invasion, as well as induced apoptosis. Most importantly, when administered intraperitoneally, combination of BSN and paclitaxel significantly decreased the tumor development in a xenograft lung cancer mouse model associated with down-modulation of phospho-STAT3, Ki- 67 and CD31. We suggest that BSN inhibits STAT3 signaling through modulation of PIAS-3 and SOCS-3, thereby attenuating tumor growth and increasing sensitivity to paclitaxel.
Source Title: Oncotarget
URI: https://scholarbank.nus.edu.sg/handle/10635/177761
ISSN: 19492553
DOI: 10.18632/oncotarget.3443
Rights: Attribution 4.0 International
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