image: Illustration of the putative interactions between Tregs, Toll-like receptors (TLRs), and microRNAs in Helicobacter-induced inflammation, highlighting the special importance of miR-155. view more
Credit: Correspondence to - Christian Prinz - christian.prinz@helios-kliniken.de
Oncotarget Volume 11, Issue 10 reported that dysregulation of noncoding micro RNA molecules has been associated with immune cell activation in the context of Helicobacter pylori-induced gastric inflammation as well as carcinogenesis, but also with downregulation of mismatch repair genes, and may interfere with immune checkpoint proteins that lead to the overexpression of antigens on gastric tumor cells.
Among the many micro RNAs involved in gastric inflammation, adenocarcinoma development and immune checkpoint regulation, mi R-155 is notable in that its upregulation is considered a key marker of chronic gastric inflammation that predisposes a patient to gastric carcinogenesis.
Dr. Christian Prinz from the Lehrstuhl für Innere Medizin1, University of Witten gGmbH, Helios Universitätsklinikum said, "Increasing evidence suggests that microRNA (miRNA) dysregulation has critical impacts on development, as well as inflammation and cancer development"
"Increasing evidence suggests that microRNA (miRNA) dysregulation has critical impacts on development, as well as inflammation and cancer development"
- Dr. Christian Prinz, Lehrstuhl für Innere Medizin1, University of Witten gGmbH, Helios Universitätsklinikum
Notably, it seems that human gastrointestinal cancer can be better classified using mi RNA expression profiles than mRNA or protein expression profiles.
Using a new bead-based flow cytometric mi RNA expression profiling method, they performed a systematic expression analysis of 217 mammalian mi RNAs from 334 samples, including multiple human cancers.
Furthermore, they successfully identified poorly differentiated tumors based on mi RNA expression profiles, whereas the classification of the same samples using messenger RNA profiles was highly inaccurate.
Many mi RNAs exhibit differential regulation in cancer, for example, mi R-34a is involved in p53-mediated apoptosis in pancreatic cancer, and nine mi RNAs are upregulated in primary breast cancer, including mi R-21, mi R-181b, and mi R-155.
The Prinz Research Team concluded in their Oncotarget Research Perspective, "clinical strategies aiming to prevent miR-155 overexpression (i. e., via silencer RNAs) may thus represent a promising method of controlling cancer growth (e. g., by allowing DNA repair), especially in pre-malignant lesions or during the early stages of gastric cancer."
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DOI - https://doi.org/10.18632/oncotarget.27520
Correspondence to - Christian Prinz - christian.prinz@helios-kliniken.de
Keywords - Helicobacter pylori, gastric inflammation, gastric cancer, microRNA, miR-155
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