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热休克蛋白 27 与唾液腺腺样囊性癌的上皮-间充质转化、干性和放射抵抗有关。

HSP27 associates with epithelial-mesenchymal transition, stemness and radioresistance of salivary adenoid cystic carcinoma.

机构信息

State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases and Department of Oral and Maxillofacial Surgery, West China Hospital of Stomatology, Sichuan University, Chengdu, China.

Department of Oral and Maxillofacial Surgery, Stomatological Hospital of Nankai University, Tianjin, China.

出版信息

J Cell Mol Med. 2018 Apr;22(4):2283-2298. doi: 10.1111/jcmm.13510. Epub 2018 Feb 9.

DOI:10.1111/jcmm.13510
PMID:29424489
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5867171/
Abstract

Epithelial-mesenchymal transition (EMT) has been shown to associate with cancer stem cells and radioresistance. However, it is obscure whether EMT itself or specific EMT regulators play causal roles in these properties of salivary adenoid cystic carcinoma (SACC). Here, we exhibited that overexpression of HSP27 drove the migration and invasion, induced EMT, as well as mediated TGF-β1-induced EMT in SACC cells, accompanying the up-regulation of Snail1 and Prrx1. Conversely, HSP27 silencing reduced the migration and invasion and contributed to MET of SACC cells. HSP27 indirectly down-regulates the expression of E-cadherin through activating Snail1 and Prrx1 expressions. Overexpression of Snail1 or Prrx1 restored the migration and invasion in HSP27 knockdown cells. Enforced expression of HSP27 enhanced colony formation, CD133 /CD44 population and radioresistance of SACC cell lines. In addition, HSP27 expression was positively associated with radioresistance and poor prognosis of SACC patients as well as with the expression of Prrx1 or Snail1 in SACC tissues. The data confirm an important function for HSP27 in SACC progression through regulating EMT and stemness, and they imply the possible association between EMT and radioresistance of SACC.

摘要

上皮-间充质转化 (EMT) 已被证明与癌症干细胞和放射抵抗有关。然而，EMT 本身或特定的 EMT 调节因子是否在唾液腺腺样囊性癌 (SACC) 的这些特性中发挥因果作用尚不清楚。在这里，我们展示了 HSP27 的过表达驱动了 SACC 细胞的迁移和侵袭，诱导了 EMT，并介导了 TGF-β1 诱导的 EMT，同时上调了 Snail1 和 Prrx1。相反，HSP27 的沉默减少了 SACC 细胞的迁移和侵袭，并促进了 MET。HSP27 通过激活 Snail1 和 Prrx1 的表达间接下调 E-钙粘蛋白的表达。Snail1 或 Prrx1 的过表达恢复了 HSP27 敲低细胞的迁移和侵袭。HSP27 的强制表达增强了 SACC 细胞系的集落形成、CD133/CD44 群体和放射抵抗性。此外，HSP27 的表达与 SACC 患者的放射抵抗性和预后不良以及 SACC 组织中 Prrx1 或 Snail1 的表达呈正相关。这些数据证实了 HSP27 通过调节 EMT 和干性在 SACC 进展中的重要作用，并暗示了 EMT 和 SACC 放射抵抗性之间的可能关联。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/f76288ff01d1/JCMM-22-2283-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/b29767f3119c/JCMM-22-2283-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/502e39bbf352/JCMM-22-2283-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/975075e70ed8/JCMM-22-2283-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/9f37696297b4/JCMM-22-2283-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/332f1e61d099/JCMM-22-2283-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/197c474870ca/JCMM-22-2283-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/f76288ff01d1/JCMM-22-2283-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/b29767f3119c/JCMM-22-2283-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/502e39bbf352/JCMM-22-2283-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/975075e70ed8/JCMM-22-2283-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/9f37696297b4/JCMM-22-2283-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/332f1e61d099/JCMM-22-2283-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/197c474870ca/JCMM-22-2283-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/96e3/5867171/f76288ff01d1/JCMM-22-2283-g007.jpg

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