A statin‐regulated microRNA represses human c‐Myc expression and function

Takwi, Apana; Li, Yan; Buscaglia, Lindsey E. Becker; Zhang, Jingwen; Choudhury, Saibyasachi N.; Park, Ae Kyung; Liu, Mofang; Young, Ken H.; Park, Woong-Yang; Martin, Robert C.

doi:10.1002/emmm.201101045

Cited by 93 publications

(88 citation statements)

References 87 publications

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“…Consistent with this, several other genes were proposed to be responsible for the tumorigenic effect of 17p deletions (55). In agreement, a recent work has demonstrated that miR33b, a statin-regulated microRNA located at 17p11.2, targets MYC and regulating c-Myc-dependent medulloblastoma proliferation (35). In any case, additional studies will be required to define the precise contributions of miR-22 loss to neoplastic growth.…”

Section: Discussionsupporting

confidence: 66%

MicroRNA 22 Regulates Cell Cycle Length in Cerebellar Granular Neuron Precursors

Berenguer

Herrera

Vuolo

et al. 2013

Molecular and Cellular Biology

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During cerebellum development, Sonic hedgehog (Shh)-induced proliferation of cerebellar granular neuronal precursors (CGNPs) is potently inhibited by bone morphogenetic proteins (BMPs). We have previously reported the upregulation of TIEG-1 and Mash1, two antimitotic factors that modulate MYCN transcription and N-Myc activity, in response to BMP2. To gain further insight into the BMP antimitotic mechanism, we used microRNA (miRNA) arrays to compare the miRNAs of CGNPs proliferating in response to Shh with those of CGNPs treated with Shh plus BMP2. The array analysis revealed that miRNA 11 (miR-22) levels significantly increased in cells treated with BMP2. Additionally, in P7 mouse cerebellum, miR-22 distribution mostly recapitulated the combination of BMP2 and BMP4 expression patterns. Accordingly, in CGNP cultures, miR-22 overexpression significantly reduced cell proliferation, whereas miR-22 suppression diminished BMP2 antiproliferative activity. In contrast to BMP2, miR-22 did not induce neural differentiation but instead significantly increased cell cycle length. Consistent with the central role played by N-myc on CGNP proliferation, Max was revealed as a direct target of miR-22, and miR-22 expression caused a significant reduction of Max protein levels and N-myc/Max-dependent promoter activity. Therefore, we conclude that, in addition to the previously described mechanisms, miR-22 plays a specific role on downstream BMPs through cerebellum growth.

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Section: Discussionsupporting

confidence: 66%

MicroRNA 22 Regulates Cell Cycle Length in Cerebellar Granular Neuron Precursors

Berenguer

Herrera

Vuolo

et al. 2013

Molecular and Cellular Biology

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“…The miR-33b gene located at 17p11.2, a genomic locus frequently deleted in group 3 MB, was recently found to be up-regulated by lovastatin and, in turn, to repress MYC expression in two human cell lines (DAOY and D283) derived from MYC-driven primary MB patient samples (Takwi et al 2012). In DAOY cells, loss of miR-512.2 correlated with increased MYC expression (Lv et al 2012).…”

Section: Microrna Regulation Of Mycmentioning

confidence: 99%

Role of MYC in Medulloblastoma

Roussel

Robinson

2013

Cold Spring Harbor Perspectives in Medicine

134

109

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Since its discovery as an oncogene carried by the avian acute leukemia virus MC29 in myelocytomatosis (Roussel et al. 1979) and its cloning (Vennstrom et al. 1982), c-MYC (MYC), as well as its paralogs MYCN and MYCL1, has been shown to play essential roles in cycling progenitor cells born from proliferating zones during embryonic development, and in all proliferating cells after birth. MYC deletion induces cell-cycle exit or cell death, depending on the cell type and milieu, whereas MYC and MYCN amplification or overexpression promotes cell proliferation and occurs in many cancers. Here, we review the relationship of MYC family proteins to the four molecularly distinct medulloblastoma subgroups, discuss the possible roles MYC plays in each of these subgroups and in the developing cells of the posterior fossa, and speculate on possible therapeutic strategies targeting MYC.

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“…This pathological upregulation is frequently due to chromosomal translocations leading to promoter rearrangement [4,5,6,7], gene amplification [7] and viral mediated insertional mutagenesis [8]. There is also evidence that c-MYC expression is suppressed by miRNAs [9,10]. …”

Section: Introductionmentioning

confidence: 99%

Down-Regulation of MiR-1294 is Related to Dismal Prognosis of Patients with Esophageal Squamous Cell Carcinoma through Elevating C-MYC Expression

Li¹,

Li²,

Rusidanmu³

et al. 2015

Cell Physiol Biochem

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Aims: Changes in the expression of microRNAs (miRNAs) have been found in many cancers. This study aimed to investigate the expression of miR-1294 in patients with esophageal squamous cell carcinoma (ESCC) and its effect on prognosis. The underlying mechanism was explored as well. Methods: We examined the expression of miRNA in human ESCC cancer tissues and adjacent non-tumor controls using quantitative reverse transcription polymerase chain reaction (qRT-PCR). And the relationship between expressions of miR-1294 and ESCC prognosis was analyzed in this study. Over-expression and knock-down methods were used to investigate the biological functions of miRNA-1294. The effect of miRNA-1294 on cell proliferation was evaluated by MTT. Besides, the function of miR-1294 on cell migration and invasion were evaluated by transwell assays. Results: MiR-1294 was significantly down-regulated in human ESCC tissues compared with the non-tumor controls tissues (P=0.014). And patients with low miR-1294 expression had a significantly poorer prognosis than those with a high miR-1294 expression (P=0.040). Negative association was defined between the expression of miR-1294 and the c-MYC expression in ESCC patients (Pearson correlation, r=-0.299, P=0.0079). Additionally, it was found that miR-1294 suppress esophageal cancer cells proliferation, migration and invasion capacity through targeting c-MYC in vitro. Conclusions: Down-regulation of miR-1294 correlates with poor prognosis of ESCC. It's partially due to the reduced function of c-MYC. This study may give insight into the understanding of pathogenesis of esophageal cancer and provide evidence for diagnosis and treatment of esophageal cancer.

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A statin‐regulated microRNA represses human c‐Myc expression and function

Cited by 93 publications

References 87 publications

MicroRNA 22 Regulates Cell Cycle Length in Cerebellar Granular Neuron Precursors

MicroRNA 22 Regulates Cell Cycle Length in Cerebellar Granular Neuron Precursors

Role of MYC in Medulloblastoma

Down-Regulation of MiR-1294 is Related to Dismal Prognosis of Patients with Esophageal Squamous Cell Carcinoma through Elevating C-MYC Expression

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