Intronic miR-301 feedback regulates its host gene, ska2, in A549 cells by targeting MEOX2 to affect ERK/CREB pathways

Cao, Guikang; Huang, Bin; Liu, Zhaohui; Zhang, Jiyan; Xu, Hua; Xia, Wei; Li, Jie; Li, Shaohua; Chen, Liucun; Ding, Hongmei; Zhao, Qiang; Fan, Ming; Shen, Beifen; Shao, Ningsheng

doi:10.1016/j.bbrc.2010.05.037

Cited by 85 publications

(72 citation statements)

References 14 publications

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“…Most of the intronic miRNAs are transcribed from the same initial transcripts and have a tight relationship with the expression of their host genes by the forecast of bioinformatics analyses 19. In addition, some miRNAs are surprisingly able to regulate their host genes in turn, for example, miR‐301 can cut down the expression of its host gene ska2 by miR‐301 inhibitor 20. The same situation occurs between IGF2 and miR‐483‐5p (the other IGF2 intronic miRNA) as well 21.…”

Section: Introductionmentioning

confidence: 99%

IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1

Zhi

Zhu

et al. 2018

J Cellular Molecular Medi

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HSCR (Hirschsprung's disease) is a serious congenital defect, and the aetiology of it remains unclear. Many studies have highlighted the significant roles of intronic miRNAs and their host genes in various disease, few was mentioned in HSCR although. In this study, miR‐483‐3p along with its host gene IGF2 (Insulin‐like growth factor 2) was found down‐regulated in 60 HSCR aganglionic colon tissues compared with 60 normal controls. FHL1 (Four and a half LIM domains 1) was determined as a target gene of miR‐483‐3p via dual‐luciferase reporter assay, and its expression was at a higher level in HSCR tissues. Here, we study cell migration and proliferation in human 293T and SH‐SY5Y cell lines by performing Transwell and CCK8 assays. In conclusion, the knockdown of miR‐483‐3p and IGF2 both suppressed cell migration and proliferation, while the loss of FHL1 leads to opposite outcome. Furthermore, miR‐483‐3p mimics could rescue the negative effects on cell proliferation and migration caused by silencing IGF2, while the FHL1 siRNA may inverse the function of miR‐483‐3p inhibitor. This study revealed that miR‐483‐3p derived from IGF2 was associated with Hirschsprung's disease by targeting FHL1 and may provide a new pathway to understand the aetiology of HSCR.

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Section: Introductionmentioning

confidence: 99%

IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1

Zhi

Zhu

et al. 2018

J Cellular Molecular Medi

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“…Relapse occurs easily, which leads to a poor prognosis (2). Previous studies have demonstrated that the differentially-expressed genes and miRNAs of adenocarcinoma may affect the development, transfer and treatment of cancer (3)(4)(5)(6)(7). In addition, there is a complex regulatory network between the TFs, miRNAs, and target and host genes in adenocarcinoma (3).…”

Section: Introductionmentioning

confidence: 99%

“…The intronic miRNAs are transcribed in parallel with the host genes (5,6). Intronic miRNAs and the host genes usually act as potential partners to achieve biological function and affect the alteration of pathways (7). These previous studies have indicated that miRNA and the miRNA host genes may affect the development of cancer.…”

Section: Introductionmentioning

confidence: 99%

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Construction and analysis of three networks of genes and microRNAs in adenocarcinoma

et al. 2015

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Abstract. Adenocarcinoma is one of the most serious diseases that threaten human health. Numerous studies have investigated adenocarcinoma and have obtained a considerable amount of data regarding genes and microRNA (miRNA) in adenocarcinoma. However, studies have only focused on one or a small number of genes and miRNAs, and the data is stored in a scattered form, making it challenging to summarize and assess the associations between the genes and miRNAs. In the present study, three networks of genes and miRNAs in adenocarcinoma were focused on. This enabled the construction of networks of elements involved in adenocarcinoma and the analysis of these networks, rather than only discussing one gene. Transcription factors (TFs), miRNAs, and target and host genes of miRNAs in adenocarcinoma, and the regulatory associations between these elements were identified in the present study. These elements and associations were then used to construct three networks, which consisted of the differentially-expressed, associated and global networks. The similarities and differences between the three networks were compared and analyzed. In total, 3 notable TFs, consisting of TP53, phosphatase and tensin homolog and SMAD4, were identified in adenocarcinoma. These TFs were able to regulate the differentially-expressed genes and the majority of the differentially-expressed miRNAs. Certain important regulatory associations were also found in adenocarcinoma, in addition to self-regulating associations between TFs and miRNAs. The upstream and downstream elements of the differentially-expressed genes and miRNAs were recorded, which revealed the regulatory associations between genes and miRNAs. The present study clearly revealed components of the pathogenesis of adenocarcinoma and the regulatory associations between the elements in adenocarcinoma. The present study may aid the investigation of gene therapy in adenocarcinoma and provides a theoretical basis for studies of gene therapy methods as a treatment for adenocarcinoma.

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“…Intronic miRNA and their host gene usually coordinately express in biological progression. They usually act as potential partner to achieve biological function and affect the alteration of pathways (Cao et al, 2010). Medical researchers have discovered many differentially expressed elements (genes and miRNAs) in adrenocortical cancer.…”

Section: Introductionmentioning

confidence: 99%

Complex Regulatory Network of MicroRNAs, Transcription Factors, Gene Alterations in Adrenocortical Cancer

Zhang

Xu²,

Wang³

et al. 2013

Asian Pacific Journal of Cancer Prevention

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Several lines of evidence indicate that cancer is a multistep process. To survey the mechanisms involving gene alteration and miRNAs in adrenocortical cancer, we focused on transcriptional factors as a point of penetration to build a regulatory network. We derived three level networks: differentially expressed; related; and global. A topology network ws then set up for development of adrenocortical cancer. In this network, we found that some pathways with differentially expressed elements (genetic and miRNA) showed some self-adaption relations, such as EGFR. The differentially expressed elements partially uncovered mechanistic changes for adrenocortical cancer which should guide medical researchers to further achieve pertinent research.

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Intronic miR-301 feedback regulates its host gene, ska2, in A549 cells by targeting MEOX2 to affect ERK/CREB pathways

Cited by 85 publications

References 14 publications

IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1

IGF2‐derived miR‐483‐3p associated with Hirschsprung's disease by targeting FHL1

Construction and analysis of three networks of genes and microRNAs in adenocarcinoma

Complex Regulatory Network of MicroRNAs, Transcription Factors, Gene Alterations in Adrenocortical Cancer

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