Epigenetically regulated<i>MIR941</i>and<i>MIR1247</i>target gastric cancer cell growth and migration

Kim, Joong Gook; Kim, Tae Oh; Bae, Jin Han; Shim, Jae Woong; Kang, Myoung Joo; Yang, Kwangmo; Ting, Angela H.; Yi, Joo Mi

doi:10.4161/epi.29007

Cited by 32 publications

(26 citation statements)

References 51 publications

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“…miRs can promote or inhibit the development and progression of human cancer (4,5). Deregulation of certain miRNAs, such as miR-10b, miR-29a, miR-145, miR-126, miR-133, miR-143, miR-148a, miR-218, miR-941, miR-1247 and miR-145, have been reported to be associated with gastric carcinoma (6)(7)(8)(9)(10)(11)(12)(13)(14)(15). miR-145 has been shown to generally act as a tumor suppressor in numerous types of human cancers, such as colorectal cancer, gastric carcinoma, bladder cancer and glioma (14,(16)(17)(18)(19)(20).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-145 inhibits the malignant phenotypes of gastric carcinoma cells via downregulation of fascin 1 expression

Xue

Zhao

Yang

et al. 2015

Molecular Medicine Reports

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MicroRNA (miR)‑145 has been demonstrated to act as a tumor suppressor, and deregulation of fascin 1 (FSCN1) has been observed in several types of human malignancy, including gastric carcinoma. However, the molecular mechanism underlying the function of miR‑145, specifically its targets in gastric carcinoma have yet to be fully elucidated. In the present study, downregulation of miR‑145 and upregulation of FSCN1 was identified in gastric carcinoma cell lines, compared with normal gastric mucosal epithelial cells. A luciferase reporter assay demonstrated that miR‑145 was able to bind to the 3'‑untranslated region of FSCN1 mRNA. Overexpression of miR‑145 led to a significant decrease in FSCN1 expression levels, whereas knockdown of miR‑145 resulted in increased FSCN1 expression levels in gastric carcinoma cells. Furthermore, overexpression of miR‑145 inhibited proliferation, migration and invasion in gastric carcinoma cells. Similar effects were also observed in gastric carcinoma cells transfected with FSCN1 small interfering RNA. In addition, overexpression of FSCN1 reversed the suppressive effects of miR‑145 upregulation on proliferation, migration and invasion in gastric carcinoma cells, suggesting that FSCN1 is indeed involved in the miR‑145‑mediated malignant phenotype of gastric carcinoma cells. The present study revealed an anti‑oncogenic role of miR‑145 in gastric carcinoma via inhibition of FSCN1, and suggested that miR‑145 may be used for the treatment of gastric carcinoma.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-145 inhibits the malignant phenotypes of gastric carcinoma cells via downregulation of fascin 1 expression

Xue

Zhao

Yang

et al. 2015

Molecular Medicine Reports

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“…Aberrant miRNA expression affects the initiation and progression of carcinogenesis, and is associates with abnormal cell proliferation, differentiation, growth, apoptosis and invasion (15). Recent advances in epigenetics have revealed that miRNA dysregulation frequently occurs in various types of neoplasm, including gastric, colon, lung and prostate cancer, as well as OS (16–20). The focus of a vast number of studies on determining the expression of miRNAs in clinical samples has identified an association between miRNA function and oncogenesis or tumor suppressor genes, which was dependent on the function of the miRNA target genes (21,22).…”

Section: Introductionmentioning

confidence: 99%

Serum microRNA-17 functions as a prognostic biomarker in osteosarcoma

Gao

Wang

et al. 2016

Oncology Letters

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MicroRNAs (miRNAs/miRs) are a class of small noncoding RNA molecules that have important roles in regulating the expression of target genes associated with the development and progression of cancer. The majority of miRNAs are expressed in a highly tissue- and region-specific manner, and released into the bloodstream as a consequences of different diseases. Furthermore, altered levels of miRNAs have been observed in several diseases, including cancer. In the present study, reverse transcription-quantitative polymerase chain reaction (RT-qPCR) demonstrated that circulating miR-17 levels were significantly upregulated in patients with osteosarcoma (OS) compared with healthy subjects. RT-qPCR also revealed that high levels of circulating miR-17 expression were inversely correlated with phosphatase and tensin homolog expression, which was identified as a target gene of miR-17 in OS tissues. Furthermore, the overall survival of patients with OS was shorter in those with high miR-17 expression compared with moderate and low expression. Taken together, these findings indicate that miR-17 may function as a useful diagnostic and prognosis biomarker or therapeutic target of OS.

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“…Epigenetically regulated miR-941 and miR-1247 are transcriptionally silenced by DNA hypermethylation. Their target mRNAs include KDM6B, TAOK1, PRDM16, RARA, STX1B, and RCC2 in gastric cancer cell lines [37]. miR-34c-5p targets 3' UTR of MAPT and the expression of miR-34c-5p is highly reduced by promoter methylation in the multidrug-resistant gastric cancer cell line, SGC-7901/VCR, and paclitaxel-resistant gastric tissues [38].…”

Section: Mirna Targets In Gastric Cancermentioning

confidence: 99%

Mechanisms of MicroRNA Deregulation and MicroRNA Targets in Gastric Cancer

Irmak-Yazicioglu

2016

Oncol Res Treat

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Reduced or increased levels of mature microRNAs (miRNAs) in tumors are often the result of deregulated transcription, epigenetic silencing, genetic loss, or defects in their biogenesis pathway in gastric cancer. Among these, Helicobacter pylori infection, epigenetic regulation and defects in the pathway of miRNA biogenesis predominate in gastric cancer [1].The miRNA profile seen in gastric cancer tissues, when compared to that of healthy controls, reveals several reasons for this. H. pylori is an etiological factor for gastric carcinogenesis. Upon infection with H. pylori, miR-21 is up-regulated while miR-218 is down-regulated in gastric epithelial tissues and AGS cells. CagA is a virulence factor of this bacteria and prevents expression of Let-7 by promoting methylation of its promoter. Tumor-associated miR-7 and miR-146a are deregulated by inflammation factors that are produced through the interaction between CagA and the host cell ( fig. 1) [2][3][4][5][6].Epigenetic regulation of miRNAs is also important for deregulation of miRNAs in gastric cancer. DNA hypomethylation and promoter methylation change the miRNA expression profile; the former causes miR-196b overexpression and the latter results in down-regulation of miR-124a [7][8]. The miR-17-92 cluster is located at a fragile site in the genome [9], and has been found to be overexpressed in many cancers including gastric cancer [10]. miR-449 inhibits cell proliferation and is down-regulated in gastric cancer [11]. E2F1 overexpression is a biomarker for gastric cancer and E2F1 transcriptionally targets and up-regulates the miR-106b/25 cluster, and up-regulated miR-106b/25 and miR-93 repress E2F1 transcription within a negative feedback loop in gastric cancer cells ( fig. 2) [12].

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Epigenetically regulatedMIR941andMIR1247target gastric cancer cell growth and migration

Abstract: These authors contributed equally to this work.

Cited by 32 publications

References 51 publications

MicroRNA-145 inhibits the malignant phenotypes of gastric carcinoma cells via downregulation of fascin 1 expression

MicroRNA-145 inhibits the malignant phenotypes of gastric carcinoma cells via downregulation of fascin 1 expression

Serum microRNA-17 functions as a prognostic biomarker in osteosarcoma

Mechanisms of MicroRNA Deregulation and MicroRNA Targets in Gastric Cancer

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