Abstract
Esophageal cancer (EC) is one of the most common mucosa-associated tumors, and is characterized by aggressiveness, poor prognosis, and unfavorable patient survival rates. As an organ directly exposed to the risk of foodborne infection, the esophageal mucosa harbors distinct populations of innate immune cells, which play vital roles in both maintenance of esophageal homeostasis and immune defense and surveillance during mucosal anti-infection and anti-tumor responses. In this review, we highlight recent progress in research into innate immune cells in the microenvironment of EC, including lymphatic lineages, such as natural killer and γδT cells, and myeloid lineages, including macrophages, dendritic cells, neutrophils, myeloid-derived suppressor cells, mast cells and eosinophils. Further, putative innate immune cellular and molecular mechanisms involved in tumor occurrence and progression are discussed, to highlight potential directions for the development of new biomarkers and effective intervention targets, which can hopefully be applied in long-term multilevel clinical EC treatment. Fully understanding the innate immunological mechanisms involved in esophageal mucosa carcinogenesis is of great significance for clinical immunotherapy and prognosis prediction for patients with EC.
Highlights
According to an analysis of 36 cancer types in 185 countries, esophageal cancer (EC) accounts for approximately 3.2% of incidence and 5.3% of mortality attributable to total cancers [1]
We review recent progress in understanding of the roles of innate immune cells, including natural killer (NK) cells, gdT cells, tumorassociated macrophages (TAMs), dendritic cells (DCs), myeloid-derived suppressor cells (MDSCs), neutrophils, mast cells (MCs) and eosinophils in the tumor microenvironment (TME) of Esophageal cancer (EC), as well as the underlying cellular and molecular mechanisms involved in tumor occurrence and progression, with the aim of providing directions for combined immunotherapy strategies and prognosis prediction
The activation of the AKT/ ERK pathway is the driving force to promote tumor cell growth, migration and invasion in EC [39, 44]. This AKT/ERK pathway can be triggered by multiple factors derived from TAMs or cancer cells themselves, involving the fibroblast growth factor 2 (FGF2)/FGF receptor 1 (FGFR1) signaling we mentioned above [39], growth differentiation factor 15 induced in TAMs and derived from cancer cells [39, 44], overexpression of ANXA10 by cancer cells interacting with CD204+ TAMs [41], and high CXCL8 expression in TAMs and cancer cells [42], which are closely correlated with tumor invasion depth, lymph node metastasis and poor prognosis and overall survival (OS) of esophageal squamous cell carcinoma (ESCC) patients
Summary
Esophageal cancer (EC) is one of the most common mucosa-associated tumors, and is characterized by aggressiveness, poor prognosis, and unfavorable patient survival rates. As an organ directly exposed to the risk of foodborne infection, the esophageal mucosa harbors distinct populations of innate immune cells, which play vital roles in both maintenance of esophageal homeostasis and immune defense and surveillance during mucosal anti-infection and anti-tumor responses. Putative innate immune cellular and molecular mechanisms involved in tumor occurrence and progression are discussed, to highlight potential directions for the development of new biomarkers and effective intervention targets, which can hopefully be applied in long-term multilevel clinical EC treatment.
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