Unraveling the Role of Epithelial–Mesenchymal Transition in Adenoid Cystic Carcinoma of the Salivary Glands: A Comprehensive Review

Abstract

Salivary adenoid cystic carcinoma (SACC) is considered a challenging malignancy; it is characterized by a slow-growing nature, yet a high risk of recurrence and distant metastasis, presenting significant hurdles in its treatment and management. At present, there are no approved targeted agents available for the management of SACC and systemic chemotherapy protocols that have demonstrated efficacy remain to be elucidated. Epithelial–mesenchymal transition (EMT) is a complex process that is closely associated with tumor progression and metastasis, enabling epithelial cells to acquire mesenchymal properties, including increased mobility and invasiveness. Several molecular signaling pathways have been implicated in the regulation of EMT in SACC, and understanding these mechanisms is crucial to identifying new therapeutic targets and developing more effective treatment approaches. This manuscript aims to provide a comprehensive overview of the latest research on the role of EMT in SACC, including the molecular pathways and biomarkers involved in EMT regulation. By highlighting the most recent findings, this review offers insights into potential new therapeutic strategies that could improve the management of SACC patients, especially those with recurrent or metastatic disease.

TAMs-derived exosomal Meg8 promotes the EMT and metastasis of SACC by regulating EGFR through sponge absorption of miR-148a-3p

“…SACC is inherently resistant to systemic chemotherapy and radiotherapy [20]. The treatment approaches of SACC metastasis are still limited and the prognosis of SACC is pessimistic [21]. Therefore, it is urgent to uncover the mechanisms of SACC metastasis to provide patients with effective anti-metastasis treatment strategies.…”

Transcription Factors and Markers Related to Epithelial–Mesenchymal Transition and Their Role in Resistance to Therapies in Head and Neck Cancers

“…They are classified as epithelial markers, e.g., Ecadherin and β-catenin, and mesenchymal markers, e.g., vimentin, fibronectin, and other EMT-associated proteins, e.g., matrix-metalloproteinases. Molecular and cellular changes associated with the EMT process include a progressive shift from epithelial polarity to loss of apical-basal polarity and enhancement of front-back polarity, changes in marker expression, such as cadherin variants from E-cadherin to N-cadherin, and adoption of a mesenchymal morphology as a result of suppression of cell-cell contacts [38][39][40]. The main protein markers and key changes in head and neck cancers associated with epithelial-mesenchymal transition (EMT).…”