Dual regulation of receptor tyrosine kinase genes EGFR and c-Met by the tumor-suppressive microRNA-23b/27b cluster in bladder cancer

Chiyomaru, Takeshi; Seki, Naohiko; Inoguchi, Satoru; Ishihara, Takeshi; Mataki, Hiroko; Matsushita, Ryo; Goto, Yusuke; Nishikawa, Rika; Tatarano, Shuichi; Iwamoto, Toshihiko; Nakagawa, Masayuki; Enokida, Hideki

doi:10.3892/ijo.2014.2752

Cited by 80 publications

(73 citation statements)

References 47 publications

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“…The expression levels of the miR-23b/27b cluster were significantly reduced in advanced bladder cancer clinical specimens [32]. Luciferase reporter assays and western blotting demonstrated that EGFR and MET transcripts were directly regulated by the miR-23b/27b cluster.…”

Section: Mirnas Targeting Egfrmentioning

confidence: 99%

RAS-MAPK pathway epigenetic activation in cancer: miRNAs in action

2015

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The highly conserved RAS-mitogen activated protein kinase (MAPK) signaling pathway is involved in a wide range of cellular processes including differentiation, proliferation, and survival. Somatic mutations in genes encoding RAS-MAPK components frequently occur in many tumors, making the RAS-MAPK a critical pathway in human cancer. Since the pioneering study reporting that let-7 miRNA acted as tumor suppressor by repressing the RAS oncogene, growing evidence has suggested the importance of miRNAs targeting the RAS-MAPK in oncogenesis. MiRNAs alterations in human cancers may act as a rheostat of the oncogenic RAS signal that is often amplified as cancers progress. However, specific mechanisms leading to miRNAs deregulation and their functional consequences in cancer are far from being fully elucidated. In this review, we provide an experimental-validated map of RAS-MAPK oncomiRs and tumor suppressor miRNAs from transmembrane receptor to downstream ERK proteins. MiRNAs could be further considered as potential genetic biomarkers for diagnosis, prognosis, or therapeutic purpose.

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Section: Mirnas Targeting Egfrmentioning

confidence: 99%

RAS-MAPK pathway epigenetic activation in cancer: miRNAs in action

2015

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“…MicroRNA‐based therapy has been suggested to be a rational and potential approach for the therapeutic targeting of EGFR . To date, a number of miRNAs, such as miR‐7 , miR‐27b and miR‐133a have been demonstrated to directly target EGFR. However, more anti‐EGFR miRNAs need to be explored, as a single mRNA can be the target of hundreds of miRNAs, and combinations of multiple tumour suppressive miRNAs targeting an individual gene might improve therapeutic efficacy by reducing resistance .…”

Section: Introductionmentioning

confidence: 99%

miR‐134 inhibits non‐small cell lung cancer growth by targeting the epidermal growth factor receptor

Qin

Wei

Zhang

et al. 2016

J Cellular Molecular Medi

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The epidermal growth factor receptor (EGFR) is frequently activated in a wide range of solid tumours and represents an important therapeutic target. MicroRNAs (miRNAs) have recently been recognized as a rational and potential modality for anti‐EGFR therapies. However, more EGFR‐targeting miRNAs need to be explored. In this study, we identified a novel EGFR‐targeting miRNA, miRNA‐134 (miR‐134), in non‐small‐cell lung cancer (NSCLC) cell lines. Luciferase assays confirmed that EGFR is a direct target of miR‐134. In addition, the overexpression of miR‐134 inhibited EGFR‐related signaling and suppressed NSCLC cells proliferation by inducing cell cycle arrest and/or apoptosis, suggesting that miR‐134 functions as a tumour suppressor in NSCLC. Further mechanistic investigation including RNAi and rescue experiments suggested that the down‐regulation of EGFR by miR‐134 partially contributes to the antiproliferative role of miR‐134. Last, in vivo experiments demonstrated that miR‐134 suppressed tumour growth of A549 xenograft in nude mice. Taken together, our findings suggest that miR‐134 inhibits non‐small cell lung cancer growth by targeting the EGFR.

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“…13,14 Decreased epidermal growth factor receptors (EGFRs) and c-Met signaling pathways are responsible for the miR-27b inhibition effect on BC proliferation, invasion, and /or metastasis. EGFR is the cell-surface receptor of the extracellular ligands-EGF family and c-Met is a hepatocyte growth factor (HGF) receptor 19 (Figure 3). …”

Section: Mir-27b Affects Cell Proliferation In Tumormentioning

confidence: 99%

“…9 MiR-27b is a familiarly dysregulated miRNA in human cancers, for example it is always up-regulated in glioma, 10 cervical cancer, 11 breast cancer (BRC) 12 and down-regulated in lung adenocarcinoma, 13,14 prostate cancer (PCa), 15 colorectal cancer (CRC), 16 acute myeloid leukemia (AML), 17 gastric cancer (GC), 18 and bladder cancer (BC). 19 Through the suppression of multiple targets, miR27b has recently emerged as a key suppressor or an oncogene in cancers. Here, we review the role of miR-27b in human cancers and partly reveal its functions in tumor progression, therapy, prognosis, as well as its prospect of clinical application based on molecular targeting therapeutic strategies.…”

Section: Introductionmentioning

confidence: 99%

Promising therapeutic role of miR-27b in tumor

Ding

Yang

et al. 2017

Tumour Biol.

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MicroRNAs are small nonprotein-encoding RNAs ranging from 18 to 25 nucleotides in size and regulate multiple biological pathways via directly targeting a variety of associated genes in cancers. MicroRNA-27b is a highly conserved MicroRNA throughout vertebrates and there are two homologs (hsa-miR-27a and hsa-miR-27b) in humans. MicroRNA27b is an intragenic microRNA located on chromosome 9q22.1 within the C9orf3 gene, clustering with miR-23b and miR-24-1 in human. As a frequently dysregulated microRNA in human cancers, microRNA-27b could function as a tumor suppressor or an oncogenic microRNA. More and more studies indicate that microRNA-27b is involved in affecting various biological processes, such as angiogenesis, proliferation, metastasis, and drug resistance, and thus may act as a promising therapeutic target in human cancers. In this review, we discuss the role of microRNA-27b in detail and offer novel insights into molecular targeting therapy for cancers.

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Dual regulation of receptor tyrosine kinase genes EGFR and c-Met by the tumor-suppressive microRNA-23b/27b cluster in bladder cancer

Cited by 80 publications

References 47 publications

RAS-MAPK pathway epigenetic activation in cancer: miRNAs in action

RAS-MAPK pathway epigenetic activation in cancer: miRNAs in action

miR‐134 inhibits non‐small cell lung cancer growth by targeting the epidermal growth factor receptor

Promising therapeutic role of miR-27b in tumor

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