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Molecular mechanism underlying epithelial‐mesenchymal transformation and cisplatin resistance in esophageal squamous cell carcinoma

Esophageal cancer (EC) occupies the seventh spot of the most prevalent malignancy cancer ailments worldwide and the sixth leading cause of cancer‐related death. Esophageal squamous cell carcinoma (ESCC) is also the most predominant histological subtype of EC, and cisplatin (DDP) is commonly used as...

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Detalles Bibliográficos
Autores principales: Song, Kewei, Ma, Chenhui, Gu, Baohong, Wang, Bofang, Ma, Huanhuan, Deng, Xiaobo, Chen, Hao
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley & Sons Australia, Ltd 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10626249/
https://www.ncbi.nlm.nih.gov/pubmed/37718469
http://dx.doi.org/10.1111/1759-7714.15094
Descripción
Sumario:Esophageal cancer (EC) occupies the seventh spot of the most prevalent malignancy cancer ailments worldwide and the sixth leading cause of cancer‐related death. Esophageal squamous cell carcinoma (ESCC) is also the most predominant histological subtype of EC, and cisplatin (DDP) is commonly used as a first‐line chemotherapeutic drug for the late advanced stages of the disease. However, the emergence of drug resistance during clinical treatment possesses a significant challenge to the therapeutic success and patient outcomes. Collectively, the epithelial‐mesenchymal transformation (EMT) is a process in which transcription factors are induced to regulate the expression of epithelial and stromal markers to promote the differentiation of epithelial cells into stromal cells. Recent studies have demonstrated a close association between EMT and chemotherapy resistance in tumor cells, with concrete evidence of reciprocal reinforcement. Therefore, in this review, we elucidate the molecular mechanism underlying ESCC, shed light on the mechanisms driving DDP resistance, and provide insights into the intricate interplay between EMT and ESCC. We have aimed to provide some new hypotheses and perspectives that may address‐inform future therapeutic strategies for ESCC treatment.