Cancer-associated fibroblasts: An emerging target against esophageal squamous cell carcinoma. (10th October 2022)

• Record Type: Journal Article
• Authors: Qiu, Liqing; Yue, Jing; Ding, Lingyu; Yin, Zihao; Zhang, Ke; Zhang, Hongfang
• Is Part Of: Cancer letters. Volume 546(2022)
• Publication Date: 2022-10-10
• Subjects: Therapy resistance -- Metastasis -- Immune escape -- CAFs activation -- CAFs-targeted therapies; Cancer -- Periodicals; Neoplasms -- Periodicals; Cancer -- Périodiques; Electronic journals; 616.994
• DOI: 10.1016/j.canlet.2022.215860
• Languages: English
• ISSNs: 0304-3835

Abstract

Abstract: Esophageal squamous cell carcinoma (ESCC) is one of the most common human malignancies worldwide and is associated with high morbidity and mortality. More than 70% of ESCC patients are diagnosed at the intermediate or advanced stage. Concurrent chemoradiotherapy is the standard treatment regimen for patients with advanced ESCC. However, ESCC patients show a poor 5-year survival rate of around 20%. Cancer-associated fibroblasts (CAFs) are a major component of the tumor microenvironment and control tumor initiation and progression. CAFs create a pro-survival and immunosuppressive microenvironment by crosstalk with cancer cells. Moreover, CAFs lead the collective invasion of cancer cells of the epithelial phenotype by remodeling the extracellular matrix. In this review, we highlight the impact of CAFs on ESCC, including induction of chemo- and radio-resistance, migration, invasion, and immune escape. The origin of CAFs and the influence of ESCC cells on CAF activation are also described. Furthermore, we highlight the clinical prospects and future trends of CAFs-targeted therapies in ESCC. A better understanding of the molecular biology of CAFs may contribute to the development of novel anti-ESCC strategies. Highlights: CAFs are very heterogeneous and abundant in the stroma of ESCC. CAFs regulate tumor behaviors via several mechanisms in ESCC. Targeting CAFs is a promising strategy for the battle against ESCC.