eISSN: 1897-4309
ISSN: 1428-2526
Contemporary Oncology/Współczesna Onkologia
Current issue Archive Manuscripts accepted About the journal Supplements Addendum Special Issues Editorial board Abstracting and indexing Subscription Contact Instructions for authors Ethical standards and procedures
SCImago Journal & Country Rank
1/2021
vol. 25
 
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abstract:
Original paper

Platelet-derived growth factor-B signalling might promote epithelial-mesenchymal transition in gastric carcinoma cells through activation of the MAPK/ERK pathway

Jiangyan Yin
1
,
Yi Guo
2
,
Zhongfu Li
2

1.
Department of Ultrasound, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
2.
Department of General Surgery, Chongqing University Central Hospital (Chongqing Emergency Medical Center), Chongqing, China
Contemp Oncol (Pozn) 2021; 25 (1): 1–6
Online publish date: 2021/03/22
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Introduction
Epithelial-mesenchymal transition (EMT) is important in the metastasis of tumours and is triggered by several key growth factors, including platelet-derived growth factor-B (PDGF-B). But, whether PDGF-B signalling promotes EMT in gastric carcinoma cells is still unknown.

Material and methods
We established 2 gastric carcinoma cell lines (MKN28 and MKN45) to stably overexpress PDGF-B by lentiviral vectors, and expression of E-cadherin, N-cadherin, and ERK-1 were detected by western blot assay. Then, PDGF-B overexpression and normal MKN28 and MKN45 cells were cocultured with PDGFR-positive fibroblast (hs738) and MAPK inhibitors were added; also, the expressions of ERK-1, E-cadherin, and N-cadherin were detected by western blot assay.

Results
After being cocultured with hs738 cells, expressions of ERK-1 and N-cadherin protein in PDGF-B overexpression MKN28 and MKN45 cells were much higher than normal MKN28 and MKN45 cells (p < 0.05), and those could be decreased by MAPK inhibitor. Also, expressions of E-cadherin protein in PDGF-B overexpression MKN28 and MKN45 cells were much lower than normal MKN28 and MKN45 cells (p < 0.05), and they could be increased by MAPK inhibitor.

Conclusions
Our data indicate that PDGF-B signalling can induce EMT in gastric carcinoma cells. Thr tumour microenvironment is imperative in the process of PDGF-B signalling inducing EMT in gastric carcinoma cells. Also, activation of MAPK/ERK pathway, which is a downstream pathway of PDGF-B signalling, might participate in this process.

keywords:

PDGF-B signalling, EMT, E-cadherin, N-cadherin, MAPK/ERK pathway

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