10q23.31

MIRN107,miR-107

Breast cancer

miR-107 was reported to be over expressed in malignant tissues from patients with advanced breast cancer, and its expression showed an inverse correlation with let-7 expression in tumors and in cancer cell lines Ectopic expression of miR-107 in human cancer cell lines led to destabilization of mature let-7, increased expression of let-7 targets, and increased malignant phenotypes (Chen et al., 2011).

Colon cancer

P53-induced miR-107 inhibited HIF-1 and tumor angiogenesis in colon cancer specimens. Furthermore, overexpression of miR-107 in tumor cells suppresses tumor angiogenesis, tumor growth, and tumor VEGF expression in mice (Yamakuchi et al., 2010).

Colorectal cancer

miR-103/107 targeted the known metastasis suppressors death-associated protein kinase (DAPK) and Krüppel-like factor 4 (KLF4) in colorectal cancer cells, resulting in increased cell motility and cell-matrix adhesion and decreased cell-cell adhesion and epithelial marker expression. miR-103/107 expression was increased in the presence of hypoxia, thereby potentiating DAPK and KLF4 downregulation and hypoxia-induced motility and invasiveness (Chen et al., 2012).

Esophageal cancer

Circulating and tissue miR-107 was found to be downregulated in esophageal cancer tissues and sera samples as compared to matched non-malignant tissues and healthy controls respectively (Sharma et al., 2013).

Gastric cancer

miR-107 expression in gastric cancer tissues was demonstrated as an independent prognostic factor for overall survival rates (OS) and disease-free survival rates (DFS). OS and DFS of patients with high miR-107 expression were significantly worse than those of patients with low miR-107 expression (Inoue et al., 2012).

Its ectopic expression reduced both mRNA and protein expression levels of CDK6, inhibited proliferation, blocked invasion of gastric cancer cells and also induced G1 cell cycle arrest (Feng et al., 2012). miR-107 expression showed significant association with depth of tumor invasion, lymph node metastasis and stage. Moreover, significant inverse correlation was found between miR-107 and DICER1 mRNA (Inoue et al., 2012) and it was demonstrated that miR107 regulates tumor invasion and metastasis in gastric cancer by targeting DICER1 (Li et al., 2011).

Glioma

miR-107 inhibited proliferation of Glioma cells (Chen et al., 2013a), downregulated expression of CDK6 and notch-2 and also inhibited glioma cell migration and invasion by modulating notch-2 expression (Chen et al., 2013b). He et al., (2013) reported that upregulation of miR-107 suppressed glioma cell growth through directly targeting SALL4, leading to the activation of FADD/caspase-8/caspase-3/caspase-7 signaling pathway of cell apoptosis.

Head and neck squamous cell carcinoma

microRNA-107 functions as a candidate tumor-suppressor gene in head and neck squamous cell carcinoma by downregulation of protein kinase Cε. Treatment with miR-107 significantly blocked cell proliferation, DNA replication, colony formation and invasion in head and neck squamous cell carcinoma (HNSCC) cell lines (Datta et al., 2012). Moreover, Lipid-based nanoparticle delivery of Pre-miR-107 inhibits the tumorigenicity of HNSCC (Piao et al., 2012).

B-cell chronic lymphocytic leukemia

Down-regulation of miRNA-107 due to epigenetic transcriptional silencing results in overexpression of its target gene PLAG1 (pleomorphic adenoma gene 1), a well known oncogenic transcription factor (Pallasch, 2009).

Lung cancer

MiR-107 suppressed cell proliferation in human non-small cell lung cancer cell lines (Takahashi et al., 2009) and induced G1 cell cycle arrest.

Neuroblastoma

miR-103 and miR-107 regulate CDK5R1 expression and their overexpression, as well as CDK5R1 silencing, caused a reduction in migration ability of neuroblastoma cells (Moncini et al., 2011).

Pancreatic cancer

Lee et al. (2009) reported that epigenetic silencing of miR-107 regulates CDK6 expression in pancreatic cancer.

Pituitary adenomas

miR-107 is overexpressed in Pituitary adenomas and may act as tumor suppressor. Pituitary tumor suppressor gene AIP (aryl hydrocarbon receptor-interacting protein) is a miR-107 target and both may have roles in tumorigenesis (Trivellin et al., 2012). Recent studies have demonstrated regulation of miR-107 by P53 tumor suppressor.

Prostate cancer

Multiple members of the miR-107 gene group repress mitogen and growth factor granulin (GRN) protein levels when transfected into prostate cancer cells (Wang et al., 2010a). GRN is dysregulated via miR-15/107 gene group in multiple human cancers, which may provide a potential common therapeutic target.

Various cancers

- Entrez Gene cytogenetic band: 10q23.31
- Ensembl cytogenetic band: 10q23.31
- HGNC cytogenetic band: 10q23.31
- Type: Cytoband, Source: UCSC, Length: 3300000, Stain: gpos75 (Database of Genomic Variants)

Hypoxia and angiogenesis

miR-107 mediates p53 regulation of hypoxic signaling and tumor angiogenesis in colon cancer. It regulates hypoxia signaling by suppressing expression of hypoxia inducible factor-1β (HIF-1β). Moreover, overexpression of miR-107 in tumor cells suppresses tumor angiogenesis, tumor growth and tumor VEGF expression in mice (Yamakuchi et al., 2010).

Metabolism

miR-107 has been implicated in metabolism of cellular lipids (Wilfred et al., 2007) and in regulation of insulin sensitivity. Caveolin-1, a critical regulator of insulin receptor has been identified as a direct target of miR-103/107 (Trajkovski et al., 2011). Human CYP2C8, a member of CYP2C subfamily of cytochrome P450 enzymes is also post-transcriptionally regulated by microRNAs 103 and 107 in human liver (Zhang et al., 2012).

Alzheimers

Expression of miR-107 decreases early in Alzheimers disease and may accelerate disease progression through regulation of beta-site amyloid precursor protein-cleaving enzyme 1 (Wang et al., 2008). Moreover, miR-107 expression tended to correlate in a negative fashion with neuritic plaque(NPs) and neurofibrillary tangle (NFTs) (Nelson and Wang, 2010) microRNAs-107/miR-103 represse translation of actin-binding protein cofilin, and their reduced levels are associated with elevated cofilin protein levels and formation of rod-like structures in a transgenic mouse model of Alzheimers disease (Yao et al., 2010).

Brain injury and neurodegenerative disease

miR-107 contributes to regulation of granulin/progranulin with implications for traumatic brain injury and neurodegenerative disease (Wang et al., 2010b).

Schizophrenia

Increased levels of miR-107 contribute to the marked loss of cortical CHRM1 in schizophrenia which may be a differentiating pathophysiology (Scarr et al., 2013).