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

Abstract

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.

Transcriptional Regulation of Epithelial to Mesenchymal Transition Related Genes by Lipopolysaccharide in Human Cervical Cancer Cell Line HeLa

“…It has shown valproic acid has the same effect on E7, and E-cadherin down-regulate, subsequently. (Faghihloo et al, 2016) MicroRNA is able to regulate EMT genes (Abba et al, 2016) Observations have shown, different microRNAs can mediate the expression of E-cadherin (Wong et al, 2014). Furthermore, in this study, LPS treatment was able to increase in amount of microRNA-9 and 192 expressions almost 12 and 8 times, respectively.…”

Role of Cadherins in Cancer—A Review

“…In addition, E-cadherin-catenin complex possesses the ability to downmodulate NF- κ B activity, which leads to inflammation-associated carcinogenesis [ 57 ]. There is also the epigenetic mechanism controlling the E-cadherin action directly associated with expression of microRNAs, microRNA-9 and microRNA-10b [ 58 ]. A recent study described tumor derived exosomes that tend to transfer EMT-related RNAs and proteins to recipient cells, mediate the instability of cadherins, and promote cancer progression [ 59 ].…”

Extracellular matrix in invasion and metastasis of oral squamous cell carcinoma

“…Epithelial cadherin also termed as E cadherin or cadherin 1 is a transmembrane glycoprotein, functioning as a cell adhesion molecule. [ 57 ] Calcium-dependent adhesion proteins (cadherins) play a critical role in cell adhesion and tissue differentiation. [ 58 ] Dysfunctional E cadherin is associated with loss of differentiation and acquisition of invasive phenotype.…”