Periostin promotes the proliferation and metastasis of osteosarcoma by increasing cell survival and activates the PI3K/Akt pathway

Chaojian Xu,Yanping Lan,Zhuangzhuang Wu,Ziyue Wang,Rong Yang,Jian Li,Zhi Tian,Huadong Zhang,Junjun Bai,Taiyong Wu,Long Zhang,Yi Feng,Jia Lv,Zhi Lv,Ruhao Zhou

doi:10.1186/s12935-021-02441-6

Chaojian Xu, Yanping Lan + Show 13 more

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https://doi.org/10.1186/s12935-021-02441-6

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BackgroundSilencing of the periostin gene (POSTN) can inhibit the biological process of several different cancers, and this inhibition may be related to down-regulation of PI3K/AKT signaling. However, the effect of POSTN on the progression, proliferation, and invasion of osteosarcoma (OS) remain unclear.MethodsWe used the Gene Expression Omnibus (GEO) database to screen datasets on in situ OS and lung metastases to identify core genes and potential pathways. We used additional bioinformatics tools to identify protein–protein interactions (PPIs) and gene networks, and selected the top seven genes whose expression had the strongest correlations with other genes.ResultsThe results indicated that POSTN was a major hub gene. Subsequent analysis of gene expression profiles showed that POSTN was highly expressed in 262 cases with sarcoma and expression was closely related to poor prognosis. We also performed enrichment analysis to identify differentially expressed genes and used real-time PCR, western blotting, and immunohistochemistry analyses to measure POSTN expression in cells and tissues. Transfection of a POSTN-shRNA plasmid into cultured OS cells (Saos-2) effectively inhibited the proliferation, invasion, and migration of these cells. Taken together, our results suggest that POSTN may play a role in promoting the proliferation and metastasis of OS by activation of the PI3K/Akt signaling pathway.ConclusionsOur results provide a preliminary characterization of the mechanism by which POSTN may regulate the migration and invasion of OS cells and also provide a theoretical basis for identifying biomarkers that have potential use for the diagnosis and treatment of OS.

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Silencing of the periostin gene (POSTN) can inhibit the biological process of several different cancers, and this inhibition may be related to down-regulation of PI3K/AKT signaling
Previous studies reported that POSTN had high expression in OS tissues, and its level in blood was negatively correlated with patient prognosis [9]
We examined the expression of POSTN in cultured OS cells and tissues at the gene and protein levels, and performed cell function and molecular biology experiments to examine the possible effect of POSTN on the proliferation and metastasis of tumor cells and the possible role of the PI3K/Akt pathway in these pathogenic processes

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Silencing of the periostin gene (POSTN) can inhibit the biological process of several different cancers, and this inhibition may be related to down-regulation of PI3K/AKT signaling. Osteosarcoma (OS) is the most common primary malignant bone tumor It has high rates of malignancy, invasion, recurrence, and metastasis, and occurs mostly in teenagers [1]. Periostin (POSTN) is a bone adhesion molecule first discovered by Takcshita et al in mouse osteoblast cell line. It is a unique extracellular matrix protein that can promote the aggregation and differentiation of osteoblasts and their precursors in the periosteum [4]. POSTN functions in the migration and adhesion of normal cells, and affects tumor cell proliferation, apoptosis, and invasion, and angiogenesis [8]. Molecular studies reported that POSTN regulated vascular endothelial cells and angiogenesis via the PI3K/AKT signaling pathway [10,11,12]

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