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.
Highlights
Epithelial–mesenchymal transition (EMT) is malignant progression in cancer, during which epithelial cells lose epithelial characteristics and gain mesenchymal feature, thereby becoming more invasive and mobile [1]
These results indicated that heat-shock protein of 27 kDa (HSP27) may be an EMT inducer and promotes the migration and invasion of salivary adenoid cystic carcinoma (SACC) cells
Our results confirmed that HSP27 may indirectly downregulate the transcription of E-cadherin, which was supported by the reports that EMT inducers such as Snail1 and Slug could transcriptionally block E-cadherin expression either directly or indirectly [30]
Summary
Epithelial–mesenchymal transition (EMT) is malignant progression in cancer, during which epithelial cells lose epithelial characteristics and gain mesenchymal feature, thereby becoming more invasive and mobile [1]. It has been hypothesized that carcinoma cells that have undergone EMT acquire cancer stem cell (CSC) properties and CSC theory suggests that a fraction of cancer cells with self-renewal and multipotential differentiation abilities are responsible for radioresistance [3, 4]. It is unclear whether EMT itself or specific EMT regulators play causal roles in these properties. Elucidating the mechanism underlying disease malignant progression is urgently needed
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