Downregulation of microRNA-1 and microRNA-145 contributes synergistically to the development of colon cancer

Xu, Xuehu; Wu, Xiaobing; Jiang, Qingping; Sun, Yan; Li, Haibo; Chen, Rong; Wu, Shangbiao

doi:10.3892/ijmm.2015.2364

Cited by 25 publications

(15 citation statements)

References 45 publications

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“…Previous findings obtained from miRNome analysis of GC patients from TCGA revealed that miR-1 was the most downregulated miRNA in GC (see Online Resource 1 in the electronic supplementary material). In this study, qPCR analysis revealed that loss of miR-1 expression was frequently observed in primary gastric tumors compared with adjacent normal tissues, which was consistent with the data observed in breast, lung, colon, and hepatocellular carcinoma [ 7 – 10 ]. Intriguingly, some studies suggested an upregulation of plasma miR-1 in GC patients, including those who developed resistance to chemoagents [ 13 , 14 ], by comparison with healthy individuals.…”

Section: Discussionsupporting

confidence: 90%

“…It ranked as the most decreased miRNA in the chromosome instability subgroup of GC, which accounted for half of the total tumors tested [ 5 ]. MiR-1, sharing a similar seed sequence with miR-206, was originally described as muscle specific, and has been shown to downregulate MET , FOXP1 , KRAS , PIK3CA , and NAIP , which are important oncogenes relating to tumorigenic properties of various cancer types [ 6 – 10 ] and even tumor-associated macrophages [ 11 ]. Microarray analysis on biopsy samples from 90 GC patients and 34 healthy volunteers by Kim et al [ 12 ] revealed that miR-1 was one of the mostly downregulated miRNAs in GC.…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-1 acts as a tumor suppressor microRNA by inhibiting angiogenesis-related growth factors in human gastric cancer

et al. 2017

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BackgroundWe recently reported that miR-1 was one of the most significantly downregulated microRNAs in gastric cancer (GC) patients from The Cancer Genome Atlas microRNA sequencing data. Here we aim to elucidate the role of miR-1 in gastric carcinogenesis.MethodsWe measured miR-1 expression in human GC cell lines and 90 paired primary GC samples, and analyzed the association of its status with clinicopathological features. The effect of miR-1 on GC cells was evaluated by proliferation and migration assay. To identify the target genes of miR-1, bioinformatic analysis and protein array analysis were performed. Moreover, the regulation mechanism of miR-1 with regard to these predicted targets was investigated by quantitative PCR (qPCR), Western blot, ELISA, and endothelial cell tube formation. The putative binding site of miR-1 on target genes was assessed by a reporter assay.ResultsExpression of miR-1 was obviously decreased in GC cell lines and primary tissues. Patients with low miR-1 expression had significantly shorter overall survival compared with those with high miR-1 expression (P = 0.0027). Overexpression of miR-1 in GC cells inhibited proliferation, migration, and tube formation of endothelial cells by suppressing expression of vascular endothelial growth factor A (VEGF-A) and endothelin 1 (EDN1). Conversely, inhibition of miR-1 with use of antago-miR-1 caused an increase in expression of VEGF-A and EDN1 in nonmalignant GC cells or low-malignancy GC cells.ConclusionsMiR-1 acts as a tumor suppressor by inhibiting angiogenesis-related growth factors in human gastric cancer. Downregulated miR-1 not only promotes cellular proliferation and migration of GC cells, but may activates proangiogenesis signaling and stimulates the proliferation and migration of endothelial cells, indicating the possibility of new strategies for GC therapy.Electronic supplementary materialThe online version of this article (doi:10.1007/s10120-017-0721-x) contains supplementary material, which is available to authorized users.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

MicroRNA-1 acts as a tumor suppressor microRNA by inhibiting angiogenesis-related growth factors in human gastric cancer

et al. 2017

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“…miRNAs play a pivotal role in cancer progression and development, and may therefore serve as novel therapeutic tools for cancer therapy [31]. Dysregulation of miR-1 is involved in carcinogenic events in various cancers, including colon cancer [36, 37], hepatocellular carcinoma [38], and esophageal squamous cell carcinoma (ESCC) [39]. In this study, we demonstrated that G6PD is also a direct target of miR-1 in cervical cancer cells.…”

Section: Discussionmentioning

confidence: 91%

miR-1 inhibits progression of high-risk papillomavirus-associated human cervical cancer by targeting G6PD

Chang

Xiao

et al. 2016

Oncotarget

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Ectopic glucose-6-phosphate dehydrogenase (G6PD) expression may contribute to tumorigenesis in cervical cancer associated with high-risk human papillomavirus (HR-HPV 16 and 18) infections. Here, we demonstrate that microRNA-1 (miR-1) in association with AGO proteins targets G6PD in HR-HPV-infected human cervical cancer cells. miR-1 inhibited expression of a reporter construct containing a putative G6PD 3′-UTR seed region and suppressed endogenous G6PD expression. Down-regulation of miR-1 increased G6PD expression in cervical cancer cells. Regression analysis revealed that miR-1 levels correlate negatively with the clinicopathologic features in HR-HPV 16/18-infected cervical cancer patients. miR-1 overexpression inhibited proliferation and promoted apoptosis in cervical cancer cells and reduced xenograft tumor growth in nude mice. Conversely, sponge-mediated miR-1 knockdown markedly increased viability and reduced apoptosis in cervical cancer cells and supported neoplasm growth. Restoration of G6PD expression partially reversed the effects of miR-1 overexpression both in vitro and in vivo. In addition, co-transfection of G6PD siRNA and miR-1 sponge partially reversed miR-1 sponge-induced reductions in cell viability and neoplasm growth. These results suggest that miR-1 suppresses the development and progression of HR-HPV 16/18-infected cervical cancer by targeting G6PD and may be a promising novel therapeutic candidate.

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“…miR-1-3p expression shows negative correlation with tumour size, degree of differentiation, lymph node metastasis and tumour/nodus/metastasis stage (TNM) [ 85 , 86 , 87 ]. In vitro, miR-1-3p suppresses cell growth, migration, motility and glycolysis by targeting VEGF [ 87 ] and notch receptor 3 ( NOTCH3 ), which is known to be crucially involved in developmental processes by controlling cell fate decisions [ 88 ] as well as hypoxia-inducible factor 1 subunit alpha ( HIF1A ) [ 89 ].…”

Section: Mirna Clusters Down-regulated In Human Crcmentioning

confidence: 99%

miRNA Clusters with Down-Regulated Expression in Human Colorectal Cancer and Their Regulation

Pidíková

Reis

Herichová

2020

IJMS

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Regulation of microRNA (miRNA) expression has been extensively studied with respect to colorectal cancer (CRC), since CRC is one of the leading causes of cancer mortality worldwide. Transcriptional control of miRNAs creating clusters can be, to some extent, estimated from cluster position on a chromosome. Levels of miRNAs are also controlled by miRNAs “sponging” by long non-coding RNAs (ncRNAs). Both types of miRNA regulation strongly influence their function. We focused on clusters of miRNAs found to be down-regulated in CRC, containing miR-1, let-7, miR-15, miR-16, miR-99, miR-100, miR-125, miR-133, miR-143, miR-145, miR-192, miR-194, miR-195, miR-206, miR-215, miR-302, miR-367 and miR-497 and analysed their genome position, regulation and functions. Only evidence provided with the use of CRC in vivo and/or in vitro models was taken into consideration. Comprehensive research revealed that down-regulated miRNA clusters in CRC are mostly located in a gene intron and, in a majority of cases, miRNA clusters possess cluster-specific transcriptional regulation. For all selected clusters, regulation mediated by long ncRNA was experimentally demonstrated in CRC, at least in one cluster member. Oncostatic functions were predominantly linked with the reviewed miRNAs, and their high expression was usually associated with better survival. These findings implicate the potential of down-regulated clusters in CRC to become promising multi-targets for therapeutic manipulation.

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Downregulation of microRNA-1 and microRNA-145 contributes synergistically to the development of colon cancer

Cited by 25 publications

References 45 publications

MicroRNA-1 acts as a tumor suppressor microRNA by inhibiting angiogenesis-related growth factors in human gastric cancer

MicroRNA-1 acts as a tumor suppressor microRNA by inhibiting angiogenesis-related growth factors in human gastric cancer

miR-1 inhibits progression of high-risk papillomavirus-associated human cervical cancer by targeting G6PD

miRNA Clusters with Down-Regulated Expression in Human Colorectal Cancer and Their Regulation

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