Interactions between E-Cadherin and MicroRNA Deregulation in Head and Neck Cancers : The Potential Interplay

Abstract EN

E-cadherin expression in the head and neck epithelium is essential for the morphogenesis and homeostasis of epithelial tissues.

The cadherin-mediated cell-cell contacts are required for the anchorage-dependent growth of epithelial cells.

Further, survival and proliferation require physical tethering created by proper cell-cell adhesion.

Otherwise, the squamous epithelial cells will undergo programmed cell death.

Head and neck cancers can escape from anoikis and enter into the epithelial-mesenchymal transition stages via the modulation of E-cadherin expression with epigenetic mechanisms.

At epigenetic level, gene expression control is not dependent on the DNA sequence.

In the context of E-cadherin regulation in head and neck cancers, 2 major mechanisms including de novo promoter hypermethylation and microRNA dysregulation are most extensively studied.

Both of them control E-cadherin expression at transcription level and subsequently hinder the overall E-cadherin protein level in the head and neck cancer cells.

Increasing evidence suggested that microRNA mediated E-cadherin expression in the head and neck cancers by directly/indirectly targeting the transcription suppressors of E-cadherin, ZEB1 and ZEB2.