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

He, Jie; Wu, Jiangbin; Xu, Ning; Xie, Weidong; Li, Mengnan; Li, Jianna; Jiang, Yu-Yang; Yang, Burton B.; Zhang, Y

doi:10.1093/nar/gks995

Cited by 66 publications

(67 citation statements)

References 57 publications

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“…One miRNA can regulate several targets in a signaling pathway, alternatively, several miRNAs can also converge on a single target [13,14,26]. Co-regulation of a group of functionally related genes to provoke detectable functional changes is a common mode of miRNA-mediated gene regulation.…”

Section: Discussionmentioning

confidence: 99%

“…As "micromanagers" of gene expression, miRNAs often have subtle influence on one single target. A variety of studies indicate that an individual miRNA may perform its function through targeting multiple components in one signaling pathway [9,12,13]. In addition, multiple miRNAs can act on the same signaling pathway or biological process [14][15][16][17].…”

Section: Introductionmentioning

confidence: 99%

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MicroRNA-188 suppresses G 1 /S transition by targeting multiple cyclin/CDK complexes

et al. 2014

Cell Communication and Signaling

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Background: Accelerated cell cycle progression is the common feature of most cancers. MiRNAs can act as oncogenes or tumor suppressors by directly modulating cell cycle machinery. It has been shown that miR-188 is upregulated in UVB-irradiated mouse skin and human nasopharyngeal carcinoma CNE cells under hypoxic stress. However, little is known about the function of miR-188 in cell proliferation and growth control. Results: Overexpression of miR-188 inhibits cell proliferation, tumor colony formation and G 1 /S cell cycle transition in human nasopharyngeal carcinoma CNE cells. Using bioinformatics approach, we identify a series of genes regulating G 1 /S transition as putative miR-188 targets. MiR-188 inhibits both mRNA and protein expression of CCND1, CCND3, CCNE1, CCNA2, CDK4 and CDK2, suppresses Rb phosphorylation and downregulates E2F transcriptional activity. The expression level of miR-188 also inversely correlates with the expression of miR-188 targets in human nasopharyngeal carcinoma (NPC) tissues. Moreover, studies in xenograft mouse model reveal that miR-188 is capable of inhibiting tumor initiation and progression by suppressing target genes expression and Rb phosphorylation.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MicroRNA-188 suppresses G 1 /S transition by targeting multiple cyclin/CDK complexes

et al. 2014

Cell Communication and Signaling

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“…Again, as stated earlier with regard to E2F3, the relative contribution, if any, of this target for the viability of cancer cells in the hypoxic niches remains elusive. The effects of miR-210 on the cells cycle may, in fact, be significantly broader, to include a group of mitosis-related genes, such as Plk1, Cdc25B, Cyclin F, Bub1B, and Fam83D (70). Whether all these represent direct targets or more indirect responders downstream of the genes discussed earlier remains unclear.…”

Section: Mir-210: a Pleiotropic Regulator Of The Cell Cyclementioning

confidence: 99%

HypoxamiRs and Cancer: From Biology to Targeted Therapy

Gee

Ivan

Calin

et al. 2014

Antioxidants & Redox Signaling

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Significance: Hypoxia is a hallmark of the tumor microenvironment and represents a major source of failure in cancer therapy. Recent Advances: Recent work has generated extensive evidence that microRNAs (miRNAs) are significant components of the adaptive response to low oxygen in tumors. Induction of specific miRNAs, collectively termed hypoxamiRs, has become an accepted feature of the hypoxic response in normal and transformed cells. Critical Issues: Overexpression of miR-210, the prototypical hypoxamiR, is detected in most solid tumors, and it has been linked to adverse prognosis in many tumor types. Several miR-210 target genes, including iron-sulfur (Fe-S) cluster scaffold protein (ISCU) and glycerol-3-phosphate dehydrogenase 1-like (GPD1L), have been correlated with prognosis in an inverse fashion to miR-210, suggesting that their downregulation by miR-210 occurs in vivo and contributes to tumor growth. Additional miRNAs are modulated by decreased oxygen tension in a more tissue-specific fashion, adding another level of complexity over the classic hypoxia-regulated gene network. Future Directions: From a biological standpoint, hypoxamiRs are emerging modifiers of cancer cell response to the adaptive challenges of the microenvironment. From a clinical perspective, assessing the status of these miRNAs may contribute to a detailed understanding of hypoxia-induced mechanisms of resistance and/or to the fine-tuning of future hypoxia-modifying therapies. Antioxid. Redox Signal. 21, 1220-1238.

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“…In contrast, overexpressed miR-210 induces cell cycle arrest in G1/G0 and G2/M phases [129]. Recent work has suggested that miR-210 may have a much broader effect on cell cycle regulation, as its expression was correlated with the downregulation of a group of mitosis-related genes, including Plk1, Cdc25B, Cyclin F, Bub1B, and Fam83D [130].…”

Section: Mir-210 Regulation Of the Cell Cyclementioning

confidence: 99%

Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response

Huang

Zuo

2014

ABBS

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Hypoxia is a key component of the tumor microenvironment and represents a well-documented source of therapeutic failure in clinical oncology. Recent work has provided support for the idea that non-coding RNAs, and in particular, microRNAs, may play important roles in the adaptive response to low oxygen in tumors. Specifically, all published studies agree that the induction of microRNA-210 (miR-210) is a consistent feature of the hypoxic response in both normal and malignant cells. miR-210 is a robust target of hypoxia-inducible factors, and its overexpression has been detected in a variety of diseases with a hypoxic component, including most solid tumors. High levels of miR-210 have been linked to an in vivo hypoxic signature and to adverse prognosis in breast and pancreatic cancer patients. A wide variety of miR-210 targets have been identified, pointing to roles in mitochondrial metabolism, angiogenesis, DNA damage response, apoptosis, and cell survival. Such targets are suspected to affect the development of tumors in multiple ways; therefore, an increased knowledge about miR-210's functions may lead to novel diagnostic and therapeutic approaches in cancer.

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

Cited by 66 publications

References 57 publications

MicroRNA-188 suppresses G 1 /S transition by targeting multiple cyclin/CDK complexes

MicroRNA-188 suppresses G 1 /S transition by targeting multiple cyclin/CDK complexes

HypoxamiRs and Cancer: From Biology to Targeted Therapy

Emerging roles of miR-210 and other non-coding RNAs in the hypoxic response

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