Periostin promotes papillary thyroid carcinoma progression by modulating mTOR/AKT pathway
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Updated: Jun 18, 2026

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
Published on: August 23, 2019
Song Wang1, Yuanchun Li1, Hong Li2
1Department of General Surgery, The Second Affiliated Hospital of Qiqihar Medical University, Qiqihar, China.
Background:
Papillary thyroid carcinoma (PTC) accounts for the prevalent type of thyroid malignancy with increasing incidence. The underlying mechanism facilitating progression is largely unknown. Periostin (POSTN) has been demonstrated to be involved in many cancers, with no clear role of POSTN in PTC progression. This study aimed to explore the function of POSTN in PTC.
Methods:
Gene expression data from The Cancer Genome Atlas (TCGA) database were analyzed, and tissue and serum samples were obtained from 30 PTC patients and 30 healthy controls. POSTN expression was evaluated using enzyme-linked immunosorbent assay (ELISA), immunohistochemistry (IHC), quantitative reverse transcription polymerase chain reaction (qRT-PCR), and Western blot. Transwell and wound healing experiments were performed to evaluate the function of POSTN in cell migratory abilities.
Results:
TCGA data revealed elevated POSTN expression in PTC tissues, particularly in advanced stages. Serum POSTN levels were markedly elevated in patients with PTC. POSTN was upregulated in PTC cells, and silencing POSTN attenuated cell proliferation as well as migratory capabilities. POSTN inhibition promoted apoptosis and autophagy in parallel, with changes linked to the AKT/mTOR pathway.
Conclusions:
POSTN is overexpressed in PTC and shows potential as a prognostic indicator. POSTN expression is associated with tumor progression by regulating AKT/mTOR signaling, which further leads to apoptosis and autophagy. POSTN may also be considered a valuable target for therapeutic strategies in PTC.
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