Different miR‐21‐3p isoforms and their different features in colorectal cancer

Abstract

MiR-21, the only microRNA (miRNA) found to be overexpressed in any type of solid tumor, its guide stand, miR-21-5p, has been studied a lot in colorectal cancer (CRC); however, few researchers focused on its passenger strand, miR-21-3p. In our study, based on The Cancer Genome Atlas (TCGA) data, we found that there were more varieties and quantities of miR-21-3p isoforms in microsatellite instability (MSI)-type CRC. We further examined the role of miR-21-3p by in vitro and in vivo studies. MiR-21-3p may be an oncogene in CRC by promoting cellular mobility through epithelial-mesenchymal transition. However, different isoforms, especially miR-21-3p 0 | 2, may be a favorable prognostic marker for CRC survival, probably due to increased complementary effect of miR-21-5p and/or target genes. Further study investigating the underlying mechanism of miRNA isoforms is needed.

The HMGA1 Pseudogene 7 Induces miR-483 and miR-675 Upregulation by Activating Egr1 through a ceRNA Mechanism

“…The results reported in Figure 1 confirm the overexpression of miR-483-5p, miR-483-3p, miR-675-5p, miR-21-3p, and the downregulation of miR-187-3p in HMGA1P7 overexpressing MEFs in comparison with the WT ones. Interestingly, these miRNAs have been associated to human cancers (such as colon, adrenocortical, oral, lung, hepatocellular, prostate, ovarian) and could be considered possible therapeutic targets [ 24 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ].…”

“…Furthermore, miR-675-5p has been found overexpressed in metastatic colon cancer cells and it is able to induce resistance to 1,25(OH)2D3 by targeting VDR [ 24 , 34 ]. In addition, also miR-21-3p has been described as oncomiR since it promotes oral cancer metastasis and colorectal cancers [ 35 , 36 ], and its silencing resulted in important reduction of ovarian and prostate cancer cell proliferation and invasion [ 37 ]. Finally, in the opposite way, miR-187-3p has been reported as oncosuppressor because of its inhibitory action on metastasis and epithelial-mesenchymal transition of hepatocellular carcinoma and non-small cell lung cancer [ 38 , 39 ].…”

miR-373 suppresses gastric cancer metastasis by downregulating vimentin

“…Increasing evidence has indicated that miRNAs may function as oncogenes or tumor suppressor genes, which are crucial in the initiation and progression of human malignancies (8). miR-21 is an extensively-researched oncogenic miRNA in a number of solid human tumors, including non-muscle-invasive bladder cancer (9), colorectal cancer (10), non-small cell lung cancer (11) and gastric cancer (12). miR-21 promoted cell growth and invasion by repressing phosphatidylinositol 3,4,5-trisphosphate 3-phosphatase and dual-specificity protein phosphatase PTEN in colorectal cancer (13), similar to the impact of miR-21 on gastric cancer (14).…”

STAT5A induced LINC01198 promotes proliferation of glioma cells through stabilizing DGCR8

“…It has been well-established that miR-21 was extensively implicated in the carcinogenesis of different organs. In consideration of passenger strand and guide stand of miR-21 that has [32], miR-21-5p, as the guide strand of miR-21, has been little described in the context of glioma outside of one recent study [33], where there has been short of functional analysis surrounding miR-21-5p that was just mentioned as one of miRNAs that target genes coding for antioxidant mitochondrial enzymes. Herein, miR-21-5p was screened out as one of differential miRNAs after DGCR8 was knocked down; displaying that silencing of miR-21-5p can profoundly slow down the growth and motilities of T87G cells.…”