Abstract
Gastrointestinal (GI) cancers, especially including esophageal, gastric and colorectal cancer, are common types of cancer with high morbidity and mortality worldwide. Despite great advances having been made for these cancers, current treatments including surgery, Radiotherapy (RT) and Chemotherapy (CT) are still far from satisfactory as these cancers are usually discovered in advanced stages that are associated with short longevity and poor outcomes. MicroRNAs (miRNAs) are short noncoding strands of RNA that regulate gene expression, affecting proliferation, development, differentiation, apoptosis, metabolism and Epithelial-mesenchymal Transition (EMT). The miR-17-92 cluster was detected as “oncomir-1”, which is involved in the onset and progression of numerous human cancers. This review presents the recent developments in knowledge about miR-17-92 clusters for diagnosing and treating GI cancers based on genetic functions, biological phenotypes, related mechanisms, biomarkers and therapeutic perspectives, which could provide a wider horizon for future use.
Highlights
Gastrointestinal cancer (GI cancer) arises from the combination of the esophagus, stomach, liver, biliary system, pancreas, small intestine, large intestine, rectum and anus, and it is related to malignant conditions of the gastrointestinal tract (GI tract) and digestive tract associated organs [1]
These highly conserved microRNAs are characterized by similar structural features, demonstrate diverse expression patterns and participate in a broad spectrum of physiological procedures including but not limited to developmental processes, proliferation, apoptosis, metabolism, differentiation, and epithelial-mesenchymal transition (EMT), and they are involved in the initiation and progression of various human cancers
Malignancy has always been recognized as a complex process involving cell proliferation, differentiation and migration, especially in gastrointestinal cancer
Summary
Gastrointestinal cancer (GI cancer) arises from the combination of the esophagus, stomach, liver, biliary system, pancreas, small intestine, large intestine, rectum and anus, and it is related to malignant conditions of the gastrointestinal tract (GI tract) and digestive tract associated organs [1]. The upregulation of miR-18a is related to the occurrence and development of gastric cancer and increases cyclin D1 by regulating the PTENPI3K-AKT-mTOR signal axis, promoting cell proliferation, and affecting chemoresistance of esophageal cancer [8]. Plasma samples were collected repeatedly over a period of 1 year to reflect the patient’s response to treatment They identified RC (rectal cancer)-specific miRNA signals, including members of the miR-17-92 cluster that distinguished responders to adjuvant chemotherapy from nonresponders. This could provide a potential treatment for patients with esophageal squamous cell carcinoma by using inhibitors of AKT-mTOR signaling to regulate the miR-1792 cluster [102]. An inhibitor of pri-miR-17-92 named MIR17PTi was developed by Morelli to induce MIR17HG
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