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PTEN通过激活Wnt/β-连环蛋白信号通路抑制AP-AR42J细胞的炎症反应、活力和迁移能力。

PTEN suppresses the inflammation, viability, and motility of AP-AR42J cells by activating the Wnt/β-catenin pathway.

作者信息

Yan Hongtao, Jiang Li, Zou Hong, Chen Tao, Liang Hongyin, Tang Lijun

机构信息

General Surgery Center of PLA, General Hospital of Western Theater Command No. 270 Rong Du Road, Jinniu District Chengdu Sichuan Province 610083 P. R. China

Cardiac Care Unit of Cardiothoracic Surgery, General Hospital of Western Theater Command Chengdu Sichuan 610083 P. R. China.

出版信息

RSC Adv. 2019 Feb 13;9(10):5460-5469. doi: 10.1039/c8ra08998a. eCollection 2019 Feb 11.

DOI:10.1039/c8ra08998a
PMID:35515912
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9060792/
Abstract

Acute pancreatitis (AP), a kind of common acute abdominal disease and typical chemical inflammation, is commonly caused by pancreatin digestion of the pancreas and surrounding tissues. The gene for phosphate and tension homology deleted on chromosome ten (PTEN) is a tumor suppressor that regulates numerous cellular processes. In the present study, we have elaborately investigated the effect of PTEN on the alleviating of AP and its underlying mechanisms. Firstly, we demonstrated an up-regulation of PTEN in the pancreatic tissues from AP rats by immunochemistry, qRT-PCR and western-blot assays. Subsequently, cellular experiments exhibited that PTEN has a significant inhibition effect on the proliferation, invasion and migration of AP cells. Further underlying mechanism studies showed that the growth of AP cells was mainly restrained by PTEN in the G1 phase through activation of the Wnt/β-catenin pathway, which can be demonstrated by the down-regulation of various pro-inflammatory cytokines such as IL-6, IL-10, TNF and IL-1β. Taking these results together, we can draw the conclusion that PTEN plays a significant role in suppressing the inflammation, viability and motility of acute pancreatitis and could be a potential target for AP therapies.

摘要

急性胰腺炎（AP）是一种常见的急性腹部疾病，属于典型的化学性炎症，通常由胰酶消化胰腺及其周围组织所致。第10号染色体缺失的磷酸酶和张力蛋白同源基因（PTEN）是一种肿瘤抑制因子，可调节众多细胞过程。在本研究中，我们深入探究了PTEN对缓解急性胰腺炎的作用及其潜在机制。首先，通过免疫组化、qRT-PCR和western-blot分析，我们证实了AP大鼠胰腺组织中PTEN表达上调。随后，细胞实验表明PTEN对AP细胞的增殖、侵袭和迁移具有显著抑制作用。进一步的机制研究表明，PTEN主要通过激活Wnt/β-连环蛋白通路在G1期抑制AP细胞生长，这可通过IL-6、IL-10、TNF和IL-1β等多种促炎细胞因子的下调得以证明。综合这些结果，我们可以得出结论，PTEN在抑制急性胰腺炎的炎症、活力和运动方面发挥着重要作用，可能成为AP治疗的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/755dfe481ca3/c8ra08998a-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/b33d991cb132/c8ra08998a-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/8cf2ccbcb367/c8ra08998a-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/e33f83da6a9b/c8ra08998a-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/487d69e1dccd/c8ra08998a-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/87d0a860140e/c8ra08998a-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/755dfe481ca3/c8ra08998a-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/b33d991cb132/c8ra08998a-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/8cf2ccbcb367/c8ra08998a-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/e33f83da6a9b/c8ra08998a-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/487d69e1dccd/c8ra08998a-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/87d0a860140e/c8ra08998a-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abf0/9060792/755dfe481ca3/c8ra08998a-f6.jpg

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