MIR152, MIR200B, and MIR338, human positional and functional neuroblastoma candidates, are involved in neuroblast differentiation and apoptosis

Ragusa, Marco; Majorana, Alessandra; Banelli, Barbara; Barbagallo, Davide; Statello, Luisa; Casciano, Ida; Guglielmino, Maria Rosa; Duro, Laura R.; Scalia, Marina; Magro, Gaetano; Pietro, Cinzia Di; Romani, Massimo; Purrello, Francesco

doi:10.1007/s00109-010-0643-0

Cited by 39 publications

(24 citation statements)

References 34 publications

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“…For example, it is down-regulated in endometrial serous adenocarcinoma (30), and HBV-related HCC (31). However, it is overexpressed in neuroblastoma (19). Therefore, conclusions regarding whether miR-152 and miR148a function as tumor suppressors have been controversial.…”

Section: Mir-152 and Mir-148a Have No Effect On Invasion Of Skov3 Cellsmentioning

confidence: 99%

“…Our previous studies have shown that miR-152 and miR148a are down-regulated in gastric cancer, when compared to their matched non-tumor adjacent tissues (NATs) (18). In neuroblastoma, miR-152 is involved in cell proliferation, neuroblast differentiation, migration, and apoptosis (19). Here, we present data showing that the expression of miR-152 and miR-148a were down-regulated in ovarian cancer tissues compared to normal ovarian tissues, although the decreased expression of miR-148a was not statistically significant.…”

Section: Introductionmentioning

confidence: 99%

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Altered expression of miR-152 and miR-148a in ovarian cancer is related to cell proliferation

Zhou

Zhao²,

Wang

et al. 2011

Oncol Rep

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Abstract. microRNAs (miRs) are endogenous small noncoding RNAs that are aberrantly expressed in various carcinomas. miR-152 and miR-148a have not been comprehensively investigated in ovarian cancer. Thus, the aim of this study was to identify the role of miR-152 and miR-148a in epithelial ovarian cancer. Total RNA was extracted from tissues of 78 patients with epithelial ovarian cancer, 17 normal ovarian epithelium tissues and two ovarian cancer cell lines. Using quantitative real-time PCR (qRT-PCR) followed by the 2 -ΔΔCT method for calculating the results, we found that the expression levels of miR-152 were significantly decreased in ovarian cancer tissues compared to normal ovarian epithelium tissues (p<0.05). However, although the expression of miR148a was also decreased in 65% of patients, no statistically significant difference in expression was found. A strong correlation was found between the expression of miR-152 and miR-148a (p<0.001, Pearson's correlation). The relationship between miR-152 or miR-148a expression levels in ovarian cancer and clinicopathological features, response to therapy and short-term survival was analyzed and the results showed that no correlation existed. In addition, we found that both miR-152 and miR-148a were down-regulated in ovarian cancer cell lines. After miR-152 or miR-148a mimics were transfected into ovarian cancer cell lines, the MTT cell proliferation assay showed that cell proliferation was significantly inhibited. Taken together, miR-152 and miR-148a may be involved in the carcinogenesis of ovarian cancer through deregulation of cell proliferation. They may be novel biomarkers for early detection or therapeutic targets of ovarian cancer. IntroductionOvarian cancer is one of the most common causes of death from gynecological malignancies. In addition, with an incidence of ~15,000 deaths annually, it is the fifth leading cause of cancer-related deaths among women in the United States (1). More than 90% of ovarian cancers are epithelial ovarian cancers (EOCs), which are derived from the ovarian surface epithelium (2). Due to a lack of effective biomarkers, ineffective tools for ovarian cancer screening, and non-specific symptoms in its early stages, more than two-thirds of patients with ovarian cancer are not diagnosed until the disease is in an advanced stage (3). Despite advances in early detection and the current standard treatment for advanced ovarian cancer, the 5-year survival rate is only 20-25% (4,5), which makes the development of alternative approaches urgent. Understanding the molecular alterations of ovarian cancer will help identify novel diagnostic markers or therapeutic targets, thereby improving the survival rates in this population of cancer patients.microRNAs (miRNAs or miRs) are a class of highly conserved, non-coding RNAs, approximately 19-25 nucleotides in length. They function as post-transcriptional regulators by binding to the 3'UTR regions of protein-encoding genes, which results in translational repression and gene silencing (6,7). Almost 30% ...

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Section: Mir-152 and Mir-148a Have No Effect On Invasion Of Skov3 Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Altered expression of miR-152 and miR-148a in ovarian cancer is related to cell proliferation

Zhou

Zhao²,

Wang

et al. 2011

Oncol Rep

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show abstract

“…In those studies, the inhibition of miR-152 was observed to cause a decrease in cell growth in Hela cells. In neuroblastoma samples, the expression of miR-152 was upregulated, and miR-152 negatively controlled apoptosis by downregulating pro-apoptotic genes such as conserved helix-loop-helix ubiquitous kinase, cullin 5 and growth arrest and DNA-damage-inducible, alpha (37). By contrast, Zhou et al (9) reported that cell proliferation was remarkably inhibited by overexpression of miR-152 in ovarian cancer cells using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay.…”

Section: Mir-152 and Its Targets Are Associated With Cell Proliferatimentioning

confidence: 99%

miR-152 as a tumor suppressor microRNA: Target recognition and regulation in cancer

Liu

Qin

et al. 2016

Oncology Letters

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Abstract. MicroRNAs (miRNAs or miRs) are endogenous translation repressors of protein-coding genes that act by binding to the 3'-untranslated region of their target genes, and may contribute to tumorigenesis by functioning as oncogenes or tumor suppressor genes. miR-152, a member of the miR-148/152 family, is aberrantly expressed in various diseases, including various types of cancer. A growing body of evidence has demonstrated that miR-152 may act as a tumor suppressor gene by regulating its target genes, which are associated with cell proliferation, migration and invasion in human cancer. In the present review, the gene structure and functions of miR-152 are discussed, and in particular, its regulatory mechanism, experimentally validated targets and tumor suppressor role in cancer, are highlighted.

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“…Besides these abnormalities, gain of chromosomes 4q, 6p, 7q, 11q and 18q, amplification of MDM2 and MYC genes, and LOH at 14q, 10q, 19q13 have also been described [3, 4]. More recently, the involvement of miRNAs in neuroblastoma pathogenesis has been assessed [5, 6]. Deregulation of miRNAs expression in malignant neuroblastomas may be due to several factors, as MYCN amplification, chromosomal deletions, or abnormal epigenetic regulation [7].…”

Section: Introductionmentioning

confidence: 99%

Altered expression of miRNAs and methylation of their promoters are correlated in neuroblastoma

Maugeri

Barbagallo

et al. 2016

Oncotarget

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Neuroblastoma is the most common human extracranial solid tumor during infancy. Involvement of several miRNAs in its pathogenesis has been ascertained. Interestingly, most of their encoding genes reside in hypermethylated genomic regions: thus, their tumor suppressor function is normally disallowed in these tumors. To date, the therapeutic role of the demethylating agent 5′-Aza-2 deoxycytidine (5'-AZA) and its effects on miRNAome modulation in neuroblastoma have not been satisfactorily explored. Starting from a high-throughput expression profiling of 754 miRNAs and based on a proper selection, we focused on miR-29a-3p, miR-34b-3p, miR-181c-5p and miR-517a-3p as candidate miRNAs for our analysis. They resulted downregulated in four neuroblastoma cell lines with respect to normal adrenal gland. MiRNAs 29a-3p and 34b-3p also resulted downregulated in vivo in a murine neuroblastoma progression model. Unlike the amount of methylation of their encoding gene promoters, all these miRNAs were significantly overexpressed following treatment with 5′-AZA. Transfection with candidate miRNAs mimics significantly decreased neuroblastoma cells proliferation rate. A lower expression of miR-181c was significantly associated to a worse overall survival in a public dataset of 498 neuroblastoma samples (http://r2.amc.nl). Our data strongly suggest that CDK6, DNMT3A, DNMT3B are targets of miR-29a-3p, while CCNE2 and E2F3 are targets of miR-34b-3p. Based on all these data, we propose that miR-29a-3p, miR-34b-3p, miR-181c-5p and miR-517a-3p are disallowed tumor suppressor genes in neuroblastoma and suggest them as new therapeutic targets in neuroblastoma.

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MIR152, MIR200B, and MIR338, human positional and functional neuroblastoma candidates, are involved in neuroblast differentiation and apoptosis

Cited by 39 publications

References 34 publications

Altered expression of miR-152 and miR-148a in ovarian cancer is related to cell proliferation

Altered expression of miR-152 and miR-148a in ovarian cancer is related to cell proliferation

miR-152 as a tumor suppressor microRNA: Target recognition and regulation in cancer

Altered expression of miRNAs and methylation of their promoters are correlated in neuroblastoma

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