MIRNA

Official Full Name

BCDIN3 domain containing RNA methyltransferase

Organism

Homo sapiens

GeneID

144233

Background

This gene encodes an RNA methyltransferase which belongs to the rossmann fold methyltransferase family, and serves as a 5'-methylphosphate capping enzyme that is specific for cytoplasmic histidyl tRNA. The encoded protein contains an S-adenosylmethionine binding domain and uses the methyl group donor, S-adenosylmethionine. This gene is overexpressed in breast cancer cells, and is related to the tumorigenic phenotype and poor prognosis of breast cancer. The encoded protein is thought to promote the cellular invasion of breast cancer cells, by downregulating the expression of tumor suppressor miRNAs through the dimethylation of the 5-monophosphate of the corresponding precursor miRNAs. [provided by RefSeq, Apr 2017]

Synonyms

BCDIN3D;

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Detailed Information

miRNAs are a class of non-coding RNAs that are about 21 to 23 nucleotides in length that can simultaneously affect multiple gene networks to coordinate powerful bio-reactions. miRNAs are present in systemic tissues and can inhibit the expression of target genes by blocking mRNA translation or degradation of mRNA by binding to the 3' untranslated region, coding region or 5' untranslated region of the target mRNA, thereby participating in cell proliferation, differentiation, and migration, metabolism and apoptosis and other growth and development processes. Studies have shown that the regulation of mRNA expression by the administration of specific miRNA analogues or inhibitors can be highly beneficial for tumors, cardiovascular and cerebrovascular diseases, autoimmune related diseases and viral infections. miRNA can significantly regulate the growth of fibroblasts and the synthesis of extracellular matrix through various molecular mechanisms, and is a key regulator of skin morphogenesis and wound healing.

Figure 1. The miRNA pathway. (Davis, G. M., et al. 2015)

Exosomal miRNA

Exosomes are a class of double-layered vesicular structural particles of approximately 30-150 nm in diameter. Studies have found that exosomal miRNAs play an important role in the process of angiogenesis. Multiple myeloma cells cultured under hypoxic conditions, significantly increased excretion secreted by normal oxygen conditions and hyperoxia conditions, and are rich in miR135a, which can significantly down-regulate the level of tumor suppressor FIH-1, thereby promoting transcription factors. HIF-1α expression is up-regulated, inducing human umbilical cord vascular endothelial cells to form a tubular structure resembling a blood vessel.

Tumor cell extracellular miRNAs have important regulatory effects on tumor microenvironment metabolism. The level of miR-122 in breast cancer cells is lower than that in normal breast epithelial cells, while the level of miR-122 in exosomes is high. This suggests that breast cancer cells may act by secreting miRNA122, which acts on the recipient cells in the tumor microenvironment. Exosomal miRNAs can indirectly promote tumor metastasis by inducing drug resistance in tumor cells. Tamoxiphenol-resistant breast cancer cells McF-7 can transmit drug resistance to tamoxiphenol-sensitive breast cancer cells McF-7 through exosomes rich in mir-221 and mir-222, leading to drug resistance in breast cancer cells.

miRNA and Tumor

The regulation of miRNAs in liver cancer is primarily achieved by targeting key genes in the signal pathway. Overexpression of miRNA-200a can significantly inhibit the metabolic capacity of hepatocellular carcinoma, and further discover that miRNA200a mainly plays a role by directly targeting growth factor receptor binding protein 2-associated protein 1 (GAB1), suggesting that miRNA200a can be studied as a new hepatic malignant tumor inhibition target in future studies. Many drug treatments work through specific targets for miRNAs. Overexpression of miRNA-494 in hepatocellular carcinoma (HCC) cell lines increases the tolerance of sorafenib via the mammalian rapamycin target protein (mTOR) signaling pathway. Sorafenib has been the first-line treatment for early HCC, but the role of sorafenib has not been well exploited due to tumor heterogeneity, innate or acquired resistance, and sorafenib and Anti-miRNA-494 binding will likely be a new target for the treatment of HCC.

The methylation of mirna-31 promoter in gastric cancer cells was negatively correlated with its surface expression. In normal gastric tissues, the expression level of mirna-31 was much higher than that of gastric cancer cells, while the methylation level was lower than that of gastric cancer cells, and vice versa. Further investigation revealed that it was histone deacetylase inhibitor 2 (HDAC2) that caused the changes in mirna-31 level, and the proliferation of cancer cells was inhibited after the down-regulation of HDAC2. These results demonstrate that mirna-31 can act as a functional inhibitor of gastric tumor cells.

References:

Davis, G. M. , Haas, M. A. , & Roger, P. . (2015). Micrornas: not “fine-tuners” but key regulators of neuronal development and function. Frontiers in Neurology, 6.
Alipoor, S. D. , Adcock, I. M. , Garssen, J. , Mortaz, E. , Varahram, M. , & Mirsaeidi, M. , et al. (2016). The roles of mirnas as potential biomarkers in lung diseases. European Journal of Pharmacology, 791, 395-404.
Sambandan, S. , Akbalik, Güney, Kochen, L. , Rinne, J. , Kahlstatt, J. , & Glock, C. , et al. (2017). Activity-dependent spatially localized mirna maturation in neuronal dendrites. Science, 355(6325), 634-637.

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