XB130 promotes proliferation and invasion of gastric cancer cellsReportar como inadecuado




XB130 promotes proliferation and invasion of gastric cancer cells - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Journal of Translational Medicine

, 12:1

Cancer microenvironment

Abstract

BackgroundXB130 has been reported to be expressed by various types of cells such as thyroid cancer and esophageal cancer cells, and it promotes the proliferation and invasion of thyroid cancer cells. Our previous study demonstrated that XB130 is also expressed in gastric cancer GC, and that its expression is associated with the prognosis, but the role of XB130 in GC has not been well characterized.

MethodsIn this study, we investigated the influence of XB130 on gastric tumorigenesis and metastasis in vivo and in vitro using the MTT assay, clonogenic assay, BrdU incorporation assay, 3D culture, immunohistochemistry and immunofluorescence. Western blot analysis was also performed to identify the potential mechanisms involved.

ResultsThe proliferation, migration, and invasion of SGC7901 and MNK45 gastric adenocarcinoma cell lines were all significantly inhibited by knockdown of XB130 using small hairpin RNA. In a xenograft model, tumor growth was markedly inhibited after shXB130-transfected GC cells were implanted into nude mice. After XB130 knockdown, GC cells showed a more epithelial-like phenotype, suggesting an inhibition of the epithelial-mesenchymal transition EMT process. In addition, silencing of XB130 reduced the expression of p-Akt-Akt, upregulated expression of epithelial markers including E-cadherin, α-catenin and β-catenin, and downregulated mesenchymal markers including fibronectin and vimentin. Expression of oncoproteins related to tumor metastasis, such as MMP2, MMP9, and CD44, was also significantly reduced.

ConclusionsThese findings indicate that XB130 enhances cell motility and invasiveness by modulating the EMT-like process, while silencing XB130 in GC suppresses tumorigenesis and metastasis, suggesting that it may be a potential therapeutic target.

KeywordsGastric cancer Adaptor protein Oncogene Epithelial-mesenchymal transition-like AbbreviationsGCGastric cancer

EMTEpithelial-mesenchymal transition

PI3KPhosphatidylinositol 3-kinase

FAKFocal adhesion kinase

shRNAShort hairpin RNA

MMPMatrix metalloproteinase

ECMExtracellular matrix

5-FU5- fluorouracil

MTTMethyl thiazolyl tetrazolium

PBSPhosphate-buffered saline

PIPropidium iodide.

Electronic supplementary materialThe online version of this article doi:10.1186-1479-5876-12-1 contains supplementary material, which is available to authorized users.

Min Shi, Dayong Zheng contributed equally to this work.

Download fulltext PDF



Autor: Min Shi - Dayong Zheng - Li Sun - Lin Wang - Li Lin - Yajun Wu - Minyu Zhou - Wenjun Liao - Yulin Liao - Qiang Zuo - Wan

Fuente: https://link.springer.com/



DESCARGAR PDF




Documentos relacionados