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缺氧-HIF-1α-骨膜蛋白轴在甲状腺癌中的作用。

Effect of hypoxia‑HIF‑1α‑periostin axis in thyroid cancer.

机构信息

Department of Obstetrics and Gynecology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Hongkou, Shanghai 200080, P.R. China.

Department of General Surgery, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Hongkou, Shanghai 200080, P.R. China.

出版信息

Oncol Rep. 2024 Apr;51(4). doi: 10.3892/or.2024.8716. Epub 2024 Feb 23.

DOI:10.3892/or.2024.8716
PMID:38391012
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10915707/
Abstract

The incidence of thyroid carcinoma (TC) has exhibited a rapid increase in recent years. A proportion of TCs exhibit aggressive behavior. The present study aimed to investigate the potential role of hypoxia‑hypoxia inducible factor 1 subunit α (HIF‑1α)‑periostin axis in the progression of TC. The upregulation of periostin and HIF‑1α expression levels was detected in 95 clinical TC tissues as compared with normal thyroid tissues. Hypoxia promoted the viability and invasion of TC cells and this effect was inhibited by the downregulation of periostin. Hypoxia also induced the Warburg effect in TC and this effect was inhibited by the silencing of periostin. Further investigations revealed that hypoxia activated HIF‑1α, which in turn regulated the expression of periostin. Immunoprecipitation and dual luciferase reporter assays demonstrated that HIF‑1α upregulated the expression of periostin by binding to the promoter of periostin. On the whole, these findings suggest the existence of a hypoxia‑HIF‑1α‑periostin axis in TC and indicate the role of this axis in the progression of TC.

摘要

近年来,甲状腺癌 (TC) 的发病率迅速上升。一部分 TC 表现出侵袭性的行为。本研究旨在探讨缺氧诱导因子 1 亚单位 α (HIF-1α)-骨膜蛋白轴在 TC 进展中的潜在作用。与正常甲状腺组织相比,在 95 例临床 TC 组织中检测到骨膜蛋白和 HIF-1α表达水平上调。缺氧促进 TC 细胞的活力和侵袭,而骨膜蛋白下调则抑制这一作用。缺氧还诱导 TC 中的瓦博格效应,而骨膜蛋白的沉默则抑制了这一效应。进一步的研究表明,缺氧激活了 HIF-1α,后者反过来调节骨膜蛋白的表达。免疫沉淀和双荧光素酶报告基因检测表明,HIF-1α 通过结合骨膜蛋白启动子上调骨膜蛋白的表达。总的来说,这些发现表明在 TC 中存在缺氧-HIF-1α-骨膜蛋白轴,并表明该轴在 TC 的进展中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/b35f1ddc2e88/or-51-04-08716-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/0b275e410e4b/or-51-04-08716-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/440b4fcf0ff1/or-51-04-08716-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/d984f77e7f7a/or-51-04-08716-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/95bff4c1e314/or-51-04-08716-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/242cf21f6016/or-51-04-08716-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/2aa7600d8679/or-51-04-08716-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/b35f1ddc2e88/or-51-04-08716-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/0b275e410e4b/or-51-04-08716-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/440b4fcf0ff1/or-51-04-08716-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/d984f77e7f7a/or-51-04-08716-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/95bff4c1e314/or-51-04-08716-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/242cf21f6016/or-51-04-08716-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/2aa7600d8679/or-51-04-08716-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d71b/10915707/b35f1ddc2e88/or-51-04-08716-g06.jpg

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