Abstract
Snail, also called Snai1, is a key regulator of EMT. Snail plays crucial roles in cancer progression, including resistance to anti-tumor drugs and invasion by various cancer cells. Slug, also known as Snai2, is also involved in the aggravation of certain tumors. In this study, we examined the roles of Slug in human oral squamous cell carcinoma (OSCC) cells. Slug is highly expressed in these cells, and Slug siRNA effectively represses anti-tumor drug resistance and invasive properties. In addition, transforming growth factor (TGF)-β upregulates the expression of Snail and Slug and promotes resistance to anti-tumor drugs in OSCC cells. Surprisingly, Slug siRNA appears to upregulate Snail expression considerably in OSCC cells. Snail siRNA also appears to upregulate Slug expression. Thus, either Slug or Snail siRNA alone partially mitigates malignant phenotypes in the presence of TGF-β, whereas both Slug and Snail siRNAs together dramatically suppress them. Therefore, Slug and Snail in tandem, but not alone, are potential therapeutic targets for nucleic acid medicines to treat oral cancer.
Highlights
The epithelial–mesenchymal transition (EMT) is an essential biological process during embryonic development, as well as during wound healing and tissue regeneration in adult tissues [1]
We observed that Slug mRNA is expressed at relatively high levels in head and neck cancer cells, compared to cancer cells from other tissues, whereas Snail mRNAs are ubiquitously expressed in the cells from almost all tissues according to Quantitative real-time PCR (qRT-PCR) analyses
We found that Slug protein levels are relatively high in human oral squamous cell carcinoma (OSCC) cells, and that cells in which Slug expression has been silenced exhibit increased sensitivity to anti-tumor drugs and reduced motile properties
Summary
The epithelial–mesenchymal transition (EMT) is an essential biological process during embryonic development, as well as during wound healing and tissue regeneration in adult tissues [1]. EMT involves the complete loss of expression of epithelial marker proteins, including E-cadherin and keratins, in epithelial cells. The expression of mesenchymal marker proteins, including N-cadherin and vimentin, is induced to complete EMT [2,3]. The pathological significance of EMT in cancer remains controversial because partial, rather than complete, EMT is crucial for promoting invasion and metastasis [2,4]. It is clear, that EMT transcription factors (EMT-TFs) promote cancer.
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