MIR1258

Locus Summary

Gene:MIR1258; microRNA 1258
Aliases: MIRN1258, mir-1258, hsa-mir-1258
Location:2q31.3
Summary:microRNAs (miRNAs) are short (20-24 nt) non-coding RNAs that are involved in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the stability and translation of mRNAs. miRNAs are transcribed by RNA polymerase II as part of capped and polyadenylated primary transcripts (pri-miRNAs) that can be either protein-coding or non-coding. The primary transcript is cleaved by the Drosha ribonuclease III enzyme to produce an approximately 70-nt stem-loop precursor miRNA (pre-miRNA), which is further cleaved by the cytoplasmic Dicer ribonuclease to generate the mature miRNA and antisense miRNA star (miRNA*) products. The mature miRNA is incorporated into a RNA-induced silencing complex (RISC), which recognizes target mRNAs through imperfect base pairing with the miRNA and most commonly results in translational inhibition or destabilization of the target mRNA. The RefSeq represents the predicted microRNA stem-loop. [provided by RefSeq, Sep 2009]
Databases:miRBase, OMIM, HGNC, Ensembl, GeneCard, Gene
Source:NCBIAccessed: 06 August, 2015

Cancer Overview

Research Indicators

Publications Per Year (1990-2015)
Graph generated 06 August 2015 using data from PubMed using criteria.

Literature Analysis

Mouse over the terms for more detail; many indicate links which you can click for dedicated pages about the topic.

Tag cloud generated 06 August, 2015 using data from PubMed, MeSH and CancerIndex

Specific Cancers (4)

Data table showing topics related to specific cancers and associated disorders. Scope includes mutations and abnormal protein expression.

Note: list is not exhaustive. Number of papers are based on searches of PubMed (click on topic title for arbitrary criteria used).

MicroRNA Function

Numbers shown below represent number of publications held in OncomiRDB database for Oncogenic and Tumor-Suppressive MicroRNAs.

TissueTarget Gene(s)Regulator(s)MIR1258 Function in CancerEffect
lung (1)
-non-small cell lung cancer (1)
inhibit cell invasion (1)
tumor-suppressive (1)
breast (1)
-breast cancer (1)
HPSE (1)
inhibit cell invasion (1)
reduce brain metastasis (1)
tumor-suppressive (1)

Source: OncomiRDB Wang D. et al. Bioinformatics 2014, 30(15):2237-2238.

Latest Publications: MIR1258 (cancer-related)

Rykov SV, Khodyrev DS, Pronina IV, et al.
[Novel miRNA genes methylated in lung tumors].
Genetika. 2013; 49(7):896-901 [PubMed] Related Publications
MicroRNAs play an important role in the regulation of expression of many genes and are involved in carcinogenesis. The regulation of miRNA gene expression can involve the methylation of promoter CpG islands. In this work, the methylation of six miRNA genes (mir-107, mir-125b-1, mir-130b, mir-137, mir-375, and mir-1258) in non-small-cell lung cancer (NSCLC) was studied for the first time by methylation-specific PCR using a representative set of specimens (39 cases). Four new genes (mir-125b-1, mir-137, mir-375, and mir-1258) methylated in primary NSCLC tumors were identified with frequencies of 56, 31, 56, and 36%, respectively. The frequencies of miRNA promoter methylation in DNA of tumors and histologically normal tissues differed significantly (P < or = 0.05 by Fisher's test). In lung tissues of 20 donors without a history of cancer, these genes were only methylated in a few cases. It was also shown that the previously unstudied promoter CpG islands of mir-107 and mir-130b were not methylated in NSCLC. The frequencies of mir-125b-1 and mir-137 methylation were shown for the first time to correlate with NSCLC progression (clinical stage and metastasis).

Tang D, Zhang Q, Zhao S, et al.
The expression and clinical significance of microRNA-1258 and heparanase in human breast cancer.
Clin Biochem. 2013; 46(10-11):926-32 [PubMed] Related Publications
OBJECTIVES: To investigate the expression profile of miR-1258 and heparanase (HPSE) in breast cancer and to assess their clinicopathological significance.
DESIGN AND METHODS: The expression levels of miR-1258 and HPSE were analyzed in normal, benign and malignant breast tissues. Their serum levels were evaluated in healthy women and in patients with benign and malignant breast disease. We studied the correlation between the expression of miR-1258 and HPSE and the clinical features presented by the patients.
RESULTS: MiR-1258 was down-regulated and HPSE was up-regulated in breast cancer, with a significant inverse correlation. A reduced miR-1258 expression and an elevated HPSE expression were associated with the lymph node status, late clinical stages, a short overall survival and a short relapse-free survival. In frozen fresh tissue samples, the miR-1258 levels in breast cancer with lymph node metastasis were significantly lower than that of breast cancer without lymph node metastasis and benign disease (BD). In contrast, the HPSE levels in breast cancer with lymph node metastasis were the highest. In serum samples, the miR-1258 levels in metastatic breast cancer (M1) were lower than that of primary breast cancer (M0) and BD. However, serum HPSE levels of M1 patients were significantly higher than that of M0 patients and BD patients.
CONCLUSIONS: MiR-1258 may play an important role in breast cancer development and progression by regulating the expression of HPSE, and they might be potential prognostic biomarkers for breast cancer.

Liu H, Chen X, Gao W, Jiang G
The expression of heparanase and microRNA-1258 in human non-small cell lung cancer.
Tumour Biol. 2012; 33(5):1327-34 [PubMed] Related Publications
This study aims to discuss the correlation between miR-1258 and the expression of heparanase (HPSE) in the cancer cells of the patients with non-small cell lung cancer (NSCLC) and the inhibition mechanism of miR-1258 on the invasion of lung cancer cell. The expression level of miR-1258 was detected by TaqMan real-time PCR assay, the expression of HPSE was detected by immunohistochemistry, and the expression level of HPSE in the cancer tissue of each case was detected by western blot and in its adjacent tissue of 53 patients with NSCLC. The influence of miR-1258 on the invasion potential of the lung cancer cell line A549 was studied with lentivirus system including cloned miR-1258 fragments subsequently. The expression of HPSE and miR-1258 in NSCLC tissue was not obviously related to patient's gender, age, differentiation extent of cancer tissue, cancer types, etc., but also staging and lymph node metastasis, and the difference was significant. Further studies showed that the relationship between the expression level of miR-1258 and the expression of HPSE was closer. The relative expression level of miR-1258 was 0.58 ± 0.07 in HPSE positive sample and 1.58 ± 0.11 in HPSE negative sample, and the difference of which was notably significant (P < 0.0001). Western blot showed that the expression level of HPSE was highly negatively related to the expression level of miR-1258. The invasion potential of A549 was notably lowered when transfected by miR-1258. The miR-1258 regulates the expression level of HPSE to influence the morbidity and metastasis of NSCLC. The miR-1258 is likely to become the key to the treatment of lung cancer metastasis.

Zhang L, Sullivan PS, Goodman JC, et al.
MicroRNA-1258 suppresses breast cancer brain metastasis by targeting heparanase.
Cancer Res. 2011; 71(3):645-54 [PubMed] Free Access to Full Article Related Publications
Heparanase (HPSE) is a potent protumorigenic, proangiogenic, and prometastatic enzyme that is overexpressed in brain metastatic breast cancer (BMBC). However, little is known about the regulation of this potential therapeutic target in BMBC, which remains very poorly managed in the clinic. We hypothesized that HPSE gene expression might be regulated by micro RNA that might be exploited therapeutically. Using miRanda and RNAhybrid, we identified miR-1258 as a candidate micro RNA that may directly target HPSE and suppress BMBC. In support of our hypothesis, we found that miR-1258 levels inversely correlated with heparanase expression, enzymatic activity, and cancer cell metastatic propensities, being lowest in highly aggressive BMBC cell variants compared with either nontumorigenic or nonmetastatic human mammary epithelial cells. These findings were validated by analyses of miR-1258 and heparanase content in paired clinical specimens of normal mammary gland versus invasive ductal carcinoma, and primary breast cancer versus BMBC. In regulatory experiments, miR-1258 inhibited the expression and activity of heparanase in BMBC cells, whereas modulating heparanase blocked the phenotypic effects of miR-1258. In functional experiments, stable expression of miR-1258 in BMBC cells inhibited heparanase in vitro cell invasion and experimental brain metastasis. Together, our findings illustrate how micro RNA mechanisms are linked to brain metastatic breast cancer through heparanase control, and they offer a strong rationale to develop heparanase-based therapeutics for treatment of cancer patients with brain metastases, BMBC in particular.

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Cite this page: Cotterill SJ. MicroRNA miR-1258, Cancer Genetics Web: http://www.cancer-genetics.org/MIR1258.htm Accessed:

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