Simultaneous Disruption of Circulating Mir-21 and Cytotoxic T Lymphocytes (Ctls): Prospective Diagnostic and Prognostic Markers for Esophageal Squamous Cell Carcinoma (Escc) Publisher Pubmed



Samiei H¹ ; Ajam F² ; Gharavi A^{3, 4} ; Abdolmaleki S⁵ ; Kokhaei P^{6, 7} ; Mohammadi S^{8, 9} ; Memarian A^{4, 10}
Source: Journal of Clinical Laboratory Analysis Published:2022

Abstract

Background: Esophageal squamous cell carcinoma (ESCC) as the most prominent type of esophageal cancer (EC) in developing countries encompasses a substantial contribution of cancer-related mortalities and morbidities. Cytotoxic T lymphocytes (CTLs) are the major subset of effector T cells against cancer. However, the microRNAs involved in the development and regulation of CTLs could be disrupted in cancers such as EC. Methods: Here, we evaluated the population of IL-10, TGF-β, IFN-γ, and IL-17a-producing CD3+CD8+ T cells, their association with the circulating levels of miR-21 and miR-29b, and their diagnostic and/or prognostic (after 160 weeks of follow-up) utilities in 34 ESCC patients (12 newly diagnosed: ND, 24 under-treatment: UT) and 34 matched healthy donors. Results: The population of IL-10 and TGF-β-producing CTLs (CD8+ Tregs) were considerably expanded, in addition to the overexpression of miR-21 in both groups (ND and UT) of ESCC patients, while the frequency of Tc17 and CD8+ Treg cells increased only in UT patients. The expression means of TGF-β and IL-10 in CTLs were considered to be excellent biomarkers (1 ≥ area under the curve: AUC ≥0.9) in distinguishing ESCC patients and associated subgroups from healthy subjects. Moreover, the lower expressions of TGF-β, IL-17a, IL-10, and IFN-γ in CTLs were associated with ESCC better prognosis. Conclusions: The association between the impaired function of CD3+ CD8+ T cell subsets and miR-21 expression could be introduced as novel therapeutic targets and powerful diagnostic and prognostic markers for ESCC. © 2021 The Authors. Journal of Clinical Laboratory Analysis published by Wiley Periodicals LLC.