The Role of E-Cadherin as a Prognostic Biomarker in Head and Neck Squamous Carcinoma: A Systematic Review and Meta-Analysis

Abstract

Aberrant expression of E-cad may be a promising prognostic signature for HNSCC, especially when it is used with other prognostic markers.

miR‑490‑5p regulates the proliferation, migration, invasion and epithelial‑mesenchymal transition of pharyngolaryngeal cancer cells by targeting mitogen‑activated protein kinase kinasekinase 9

“…MMP-9 is one of the invasion and migration marker proteins, and a number of studies have demonstrated that the upregulation of MMP-9 could enhance the migration and invasion of a variety of cancer cells including gastric cancer, esophageal squamous cell cancer and oral cancer (29-31). E-cadherin not only inhibits the communication between tumor cells, but also the movement and invasion of tumors (32). The downregulation of E-cadherin could significantly lower the risk of EMT of tumor cells (32,33).…”

“…E-cadherin not only inhibits the communication between tumor cells, but also the movement and invasion of tumors (32). The downregulation of E-cadherin could significantly lower the risk of EMT of tumor cells (32,33). vimentin is one of the cytoskeletal proteins and is expressed mainly in cells derived from mesoderm, which is considered to be a key factor in EMT (34,35).…”

ZEB1 and oncogenic Ras constitute a regulatory switch for stimulus‐dependent E‐cadherin downregulation

“…Furthermore, its downregulation facilitates immune escape 6 and leads to drug resistance in epidermal growth factor receptor‐mutated cancer cells 7 . Consistently, loss of E‐cadherin expression is often detected in invasive cancer cells and correlates with a poor prognosis in some types of cancers 8‐10 . However, there is also a recent emergence of reports of contrasting effects on cancer progression.…”

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“…[7] Oxidative stress following the formation of free radicals is thought to play a major role in the neuropathology of the disease. [8,[25][26][27][28][29] The intrastriatal injection of 6-hydroxydopamine (6-OHDA) at a predetermined dosage in rats results in progressive and gradual loss of dopaminergic neurons in the substantia nigra whose trend is similar to the neuropathology of the Parkinson's disease and is considered as a valid empirical model for showing the stages of the onset of the disease. [9,[30][31][32][33][34] The neurotoxin 6-OHDA through producing free radicals, which in turn have cytotoxic effect, disrupts calcium homeostasis by increasing the penetration or exacerbation of release from intracellular reserves, [10,35,36] affecting the genetic regulation and induction of apoptosis [11,[37][38][39][40] and causing neuronal death.…”