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PlGF knockdown inhibited tumor survival and migration in gastric cancer cell via PI3K/Akt and p38MAPK pathways
Author(s) -
Akrami Hassan,
Mahmoodi Fatemeh,
Havasi Somaye,
Sharifi Amene
Publication year - 2016
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3176
Subject(s) - gene knockdown , protein kinase b , pi3k/akt/mtor pathway , cd44 , cancer research , small interfering rna , apoptosis , cell growth , microbiology and biotechnology , signal transduction , chemistry , biology , cell culture , cell , transfection , biochemistry , genetics
The molecular signalling of placental growth factor (PlGF), a member of the vascular endothelial growth factor family, was not uncovered in human adenocarcinoma gastric cell line (AGS). The purpose of this study was to examine the inhibitory effects of PlGF knockdown on cell proliferation, apoptosis and migration through p38 mitogen‐activated protein kinase (p38MAPK) and PI3K pathways in human adenocarcinoma gastric cell line (AGS). To study PlGF knockdown effect, AGS cells were treated with 40 pmol of small interfering RNA (siRNA) related to PlGF gene and also a scrambled siRNA as control. Trypan Blue and Anexin V staining of AGS cells treated with PlGF ‐specific siRNA showed induction of apoptosis. Wound healing assay and zymography indicated that cellular migration and matrix metalloproteinases activities were reduced in response to PlGF knockdown. Phosphorylation of Akt and p38MAPK was reduced in AGS cells treated with PlGF ‐specific siRNA. PlGF knockdown decreased transcripts of PI3K , Akt , p38MAPK , PCNA , Caspase‐3 , OCT3 / OCT4 and CD44 , but elevated p53 and SOX2 transcripts. Our results indicated that PlGF knockdown decreased migration and induced apoptosis through PI3K/Akt1 and p38MAPK signal transduction in AGS cells. Copyright © 2016 John Wiley & Sons, Ltd.