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MiR-210 disturbs mitotic progression through regulating a group of mitosis-related genes.

Abstract
MiR-210 is up-regulated in multiple cancer types but its function is disputable and further investigation is necessary. Using a bioinformatics approach, we identified the putative target genes of miR-210 in hypoxia-induced CNE cells from genome-wide scale. Two functional gene groups related to cell cycle and RNA processing were recognized as the major targets of miR-210. Here, we investigated the molecular mechanism and biological consequence of miR-210 in cell cycle regulation, particularly mitosis. Hypoxia-induced up-regulation of miR-210 was highly correlated with the down-regulation of a group of mitosis-related genes, including Plk1, Cdc25B, Cyclin F, Bub1B and Fam83D. MiR-210 suppressed the expression of these genes by directly targeting their 3'-UTRs. Over-expression of exogenous miR-210 disturbed mitotic progression and caused aberrant mitosis. Furthermore, miR-210 mimic with pharmacological doses reduced tumor formation in a mouse metastatic tumor model. Taken together, these results implicate that miR-210 disturbs mitosis through targeting multi-genes involved in mitotic progression, which may contribute to its inhibitory role on tumor formation.
AuthorsJie He, Jiangbin Wu, Naihan Xu, Weidong Xie, Mengnan Li, Jianna Li, Yuyang Jiang, Burton B Yang, Yaou Zhang
JournalNucleic acids research (Nucleic Acids Res) Vol. 41 Issue 1 Pg. 498-508 (Jan 07 2013) ISSN: 1362-4962 [Electronic] England
PMID23125370 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • 3' Untranslated Regions
  • MIRN210 microRNA, human
  • MicroRNAs
Topics
  • 3' Untranslated Regions
  • Animals
  • Cell Hypoxia
  • Cell Line, Tumor
  • Cell Proliferation
  • Cell Transformation, Neoplastic (genetics, pathology)
  • Chromosome Segregation
  • Down-Regulation
  • Gene Expression Regulation, Neoplastic
  • Humans
  • Mice
  • Mice, Nude
  • MicroRNAs (metabolism)
  • Mitosis (genetics)
  • Neoplasm Metastasis

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