Src homology 2 domain–containing inositol-5-phosphatase and CCAAT enhancer-binding protein β are targeted by miR-155 in B cells of Eμ-MiR-155 transgenic mice

Costinean, Stefan; Sandhu, Sukhinder K.; Pedersen, Irene M.; Tili, Esmerina; Trotta, Rossana; Perrotti, Danilo; Ciarlariello, David; Neviani, Paolo; Harb, Jason G.; Kauffman, Lauren Rachel; Shidham, Aaditya; Croce, Carlo M.

doi:10.1182/blood-2009-05-220814

Cited by 279 publications

(236 citation statements)

References 36 publications

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“…We hypothesized that the loss of SHIP-1 might also be due to translational repression by miRs. miR-155 has recently been shown to suppress SHIP-1 expression by binding to its 3 0 untranslated region (UTR) (Costinean et al, 2009;O'Connell et al, 2009;Pedersen et al, 2009;Yamanaka et al, 2009). Three different internet-based miR prediction programs (http://www.microrna.org, http://www.targetscan.org, and http://mirnamap.mbc.nctu.edu.tw) predicted that SHIP-1 could be targeted not only by miR-155 but also by miR-210.…”

Section: Resultsmentioning

confidence: 99%

“…Increased levels of miR-155 were also found among high-risk, not low-risk, MDS patients (Pons et al, 2009). Downregulation of SHIP-1 expression by miR-155 activates the PI 3 0 kinase/Akt pathway (Costinean et al, 2009;Pedersen et al, 2009 (Rosenfeld and List, 2000). Aberrant expression of miR-155 has recently been found in natural killer leukemia/lymphoma cells that display increased level of phospho-Akt (Yamanaka et al, 2009).…”

Section: Discussionmentioning

confidence: 99%

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Loss of SHIP-1 protein expression in high-risk myelodysplastic syndromes is associated with miR-210 and miR-155

et al. 2012

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The myelodysplastic syndromes (MDSs) comprise a group of disorders characterized by multistage progression from cytopenias to acute myeloid leukemia (AML). They display exaggerated apoptosis in early stages, but lose this behavior during evolution to AML. The molecular basis for loss of apoptosis is unknown. To investigate this critical event, we analyzed phosphatidylinositol (PI) 3 0 kinase signaling, implicated as a critical pathway of cell survival control in epithelial and hematological malignancies. PI 3 0 kinase activates Akt through its production of 3 0 phosphoinositides. In turn, the phosphoinositides are dephosphorylated by two lipid phosphatases, PTEN and SHIP-1, in myeloid cells. We studied primary MDS-enriched bone marrow cells and bone marrow sections by western blotting, immunohistochemistry, immunocytochemistry and quantitative PCR for components of the SHIP/PTEN/PI 3 0 kinase signaling circuit. We reported constitutively activated Akt, variable levels of PTEN and uniformly decreased SHIP-1 expression in MDS progenitor cells. Overexpression of SHIP-1, but not the phosphatase-deficient form, inhibited myeloid leukemic growth. Levels of microRNA (miR)-210 and miR-155 transcripts, which target SHIP-1, were increased in CD34 þ MDS cells compared with their normal counterparts. Direct binding of miR-210 to the 3 0 untranslated region of SHIP-1 was confirmed by luciferase reporter assay. Transfection of a myeloid cell line with miR-210 resulted in loss of SHIP-1 protein expression. These data suggest that miR-155 and miR-210/SHIP-1/Akt pathways could serve as clinical biomarkers for disease progression, and that miR-155 and miR-210 might serve as novel therapeutic targets in MDS.

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Section: Resultsmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Loss of SHIP-1 protein expression in high-risk myelodysplastic syndromes is associated with miR-210 and miR-155

et al. 2012

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“…14 Enhanced B-cell proliferation was also observed in miR-155 transgenic mice, which finally developed acute lymphoblastic leukemia (ALL) and high-grade lymphoma. 15 Deletion of miR-145 and miR-146a genes on chromosome 5q was associated in patients with myelodysplastic syndrome. 16 Both miRNAs are abundantly expressed in normal hematopoietic stem/progenitor cells.…”

Section: Mirna (Mis)management Of Hematopoiesismentioning

confidence: 99%

MicroRNAs in acute leukemia: from biological players to clinical contributors

2011

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MicroRNAs (miRNAs) are involved in the management of hematopoiesis. As a consequence, miRNA dysregulation causes disruption of the hematopoietic system and leukemia may arise. We here comprehensively discuss miRNAs found discriminative for cytogenetic and molecular subtypes of acute leukemia. These miRNAs are either known miRNAs involved in leukemogenesis with proven tumor suppressor or oncogenic activities or are newly identified by high-throughput sequencing with yet unknown function. Furthermore, forces are outlined that drive aberrant miRNA function, which include genetic abnormalities (for example, deletions, translocations and mutations) and epigenetic aberrations (for example, aberrant DNA methylation or histone modifications). Interestingly, leukemia-silenced miRNAs can be re-expressed upon treatment with de-methylating agents. Targeting miRNA expression may serve a therapeutical role, albeit at present this way of targeted therapy is in its infancy. However, emerging knowledge about the biology of miRNAs in leukemia may result into a role for these miRNAs in the diagnosis and treatment of acute leukemia.

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“…SHIP is another lipid phosphatase that inhibits the generation of PIP3. The expression of SHIP can be suppressed by miR-155 in leukemia and lymphoma [86] .…”

Section: Pi3k/akt Pathwaymentioning

confidence: 99%

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

Liang

2011

Acta Pharmacol Sin

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The cell cycle, which is precisely controlled by a number of regulators, including cyclins and cyclin-dependent kinases (CDKs), is crucial for the life cycle of mammals. Cell cycle dysregulation is implicated in many diseases, including cancer. Recently, compelling evidence has been found that microRNAs play important roles in the regulation of cell cycle progression by modulating the expression of cyclins, CDKs and other cell cycle regulators. Herein, the recent findings on the regulation of the cell cycle by microRNAs are summarized, and the potential implications of miRNAs in anti-cancer therapies are discussed.

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Src homology 2 domain–containing inositol-5-phosphatase and CCAAT enhancer-binding protein β are targeted by miR-155 in B cells of Eμ-MiR-155 transgenic mice

Cited by 279 publications

References 36 publications

Loss of SHIP-1 protein expression in high-risk myelodysplastic syndromes is associated with miR-210 and miR-155

Loss of SHIP-1 protein expression in high-risk myelodysplastic syndromes is associated with miR-210 and miR-155

MicroRNAs in acute leukemia: from biological players to clinical contributors

Macro-management of microRNAs in cell cycle progression of tumor cells and its implications in anti-cancer therapy

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