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Expression profile of lncRNAs and miRNAs in esophageal cancer: Implications in diagnosis, prognosis, and therapeutic response
Author(s) -
GhafouriFard Soudeh,
Shoorei Hamed,
Dashti Sepideh,
Branicki Wojciech,
Taheri Mohammad
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29825
Subject(s) - microrna , wnt signaling pathway , biology , esophageal cancer , cancer , context (archaeology) , cancer research , signal transduction , bioinformatics , computational biology , gene , genetics , paleontology
Esophageal cancer is the seventh most common cancer worldwide. Although a number of environmental and lifestyle‐related risk factors have been identified for this kind of cancer, the exact molecular mechanisms of tumor evolution have not been clarified yet. Long noncoding RNAs (lncRNAs) and microRNAs (miRNAs) as important regulators of gene expression and chromatin configuration have essential roles in the pathogenesis of esophageal cancer. They have been shown to alter the function of cancer‐related signaling pathways such as phosphoinositide 3‐kinase/protein kinase B and Wnt pathway, thus they might modulate the response of patients to pathway‐targeted therapies. Moreover, a number of lncRNAs, such as AFAP1‐AS1 , UCA1 , HOTAIR , LOC285194 , and TUSC7 , are involved in conferring chemoresistant/radioresistant in esophageal cancer cells. A complex network of interaction exists between lncRNAs and miRNAs in the context of esophageal cancer. Finally, various panels of lncRNAs and miRNAs have been introduced that can predict the survival of esophageal cancer patients. In this review article, we summarize the recent findings regarding the role of miRNAs and lncRNAs in the pathogenesis of esophageal cancer with the special focus on their regulatory roles on signaling pathways, their potential as diagnostic/prognostic markers, and their relevance with therapeutic response.