HSP 27 associates with epithelial–mesenchymal transition, stemness and radioresistance of salivary adenoid cystic carcinoma
Authors: Jiashun Wu
Surui Sheng
Ya-Ling Tang
Wei Chen
Xiaolei Gao
Ya-Jie Tang
Xiaohua Ren
Qianming Chen
Xin-Hua Liang
Xiao Cen
Shasha Wang
Journal: Journal of Cellular and Molecular Medicine (2018)
Discipline: MOLECULAR BIOLOGY & GENETICS
Keywords: EMT; HSP27; metastasis; radioresistance; salivary adenoid cystic carcinoma (SACC).
Affiliations: 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., Department of Stomatology, Sichuan Academy of Medical Sciences and Sichuan People's Hospital, Chengdu, China., Key Laboratory of Fermentation Engineering (Ministry of Education), Hubei Provincial Cooperative Innovation Center of Industrial Fermentation, Hubei Key Laboratory of Industrial Microbiology, Hubei University of Technology, Wuhan, China., Department of Oral Pathology, West China Hospital of Stomatology (Sichuan University), Chengdu, China.

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. 

Retracted: No

PubPeer comments:
 Two images in Figure 1B overlap. ![file] , 
 Two images in Figure 2C overlap ![file] , 
 In Figure 3A, two transwell images are the same image and its mirrored version. ![file] , 
 Figure 5A apparently shows rats and dissected tumors. There are a couple of things strange here. 1. All animals and dissected tumors are kind of floating in the air without any background of a pad sheet or any surface. How were the photos taken? Was any software used to erase the background? 2. The dissected tumors were almost perfect fit when superimposing their semi-transparent negatives onto the rats, suggesting some kind of digital tool was used to create the tumor images, rather than a plain photo of the dissected tumors. Were the tumors, after PHYSICALLY dissected from the animals (I suppose that was actually done?), photographed? Can the authors upload the photos showing the dissected tumors rather than a digitally stripped tumor images obtained with the help of magic Lasso tool in Photoshop (or similar) ? ![file] , 
 There likely are duplications between Figure 1F and Figure 6B, marked by boxes with same color ![file] ,