Abstract:Objective. MiR-491-3p, as a tumor suppressor miRNA, was found decreased in many solid tissues. In this study, we aim to investigate miR-491-3p expression in gastric cancer with or without lymph node metastasis (LNM). Methods. GSE173215 dataset from Gene Expression Omnibus (GEO) was used to measure miRNA expression from tissue samples of gastric cancer patients. Moreover, gastric tumor tissues (non-LNM: n = 78; LNM: n = 68) were obtained to detect the miR-491-3p expression. Receiver operating characteristic (RO… Show more
“…LNM in GC is a complex and orderly process, involving the acquisition of invasive phenotype at the primary tumor site, preparation of metastasis channels, regulation of immune microenvironment, preparation of microenvironment at the metastasis site, and other pathological processes [5][6][7][8]. In-depth exploration and study of the pathological mechanism in the process of LNM would better understand the biological behavior of GC and provide more targets for the diagnosis and treatment [9,10].…”
“…LNM in GC is a complex and orderly process, involving the acquisition of invasive phenotype at the primary tumor site, preparation of metastasis channels, regulation of immune microenvironment, preparation of microenvironment at the metastasis site, and other pathological processes [5][6][7][8]. In-depth exploration and study of the pathological mechanism in the process of LNM would better understand the biological behavior of GC and provide more targets for the diagnosis and treatment [9,10].…”
“…MiR-491-3p is one of the mature products of miR-491. Recently, miR-491-3p has been reported to be involved in the progression of several cancers, such as retinoblastoma, tongue cancer, glioblastoma, and gastric cancer ( Hu et al, 2021 ; Zheng et al, 2015 ; Li et al, 2015 ; Yu & Luo, 2022 ). Furthermore, it has been demonstrated that miR-491 facilitates CRC cell apoptosis by reducing Bcl-XL expression ( Nakano et al., 2010 ).…”
Colorectal carcinoma (CRC) is the second most frequent cancer worldwide. MiR-491-3p, a tumor-suppressive microRNA (miRNA, miR), has been revealed to be abnormally expressed in CRC tissues. Meanwhile, up-regulated ubiquitous mitochondrial creatine kinase (uMtCK) contributes to CRC cell proliferation. Here we aim to explore whether aberrant miR-491-3p expression promotes CRC progression through regulating uMtCK. To this end, miR-491-3p and uMtCK levels were assessed in CRC tissues using quantitative real-time PCR (qRT-PCR). The biological roles of miR-491-3p and uMtCK in regulating CRC growth were evaluated using colony formation assay and mouse Xenograft tumour model. We found that miR-491-3p expression was decreased in CRC tissues compared with matched para-cancerous tissues, whereas uMtCK expression was increased. Functionally, miR-491-3p overexpression repressed SW480 cell growth, whereas miR-491-3p depletion accelerated SW620 cell proliferation and growth. Inversely, uMtCK positively regulated CRC cell proliferation. Mechanistically, miR-491-3p post-transcriptionally downregulated uMtCK expression by binding to 3’-UTR of uMtCK. Consequently, restoring uMtCK expression markedly eliminated the role of miR-491-3p in suppressing CRC growth. Collectively, miR-491-3p functions as a tumour suppressor gene by repressing uMtCK, and may be a potential target for CRC treatment.
“…This article has been retracted by Hindawi following an investigation undertaken by the publisher [ 1 ]. This investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process: Discrepancies in scope Discrepancies in the description of the research reported Discrepancies between the availability of data and the research described Inappropriate citations Incoherent, meaningless and/or irrelevant content included in the article Peer-review manipulation …”
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confidence: 99%
“…Tis article has been retracted by Hindawi following an investigation undertaken by the publisher [1]. Tis investigation has uncovered evidence of one or more of the following indicators of systematic manipulation of the publication process:…”
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