Expression profile of CREB knockdown in myeloid leukemia cells

Pellegrini, Matteo; Cheng, Jerry C.; Voutila, Jon; Judelson, Dejah R.; Taylor, Julie; Nelson, Stanley F.; Sakamoto, Kathleen M.

doi:10.1186/1471-2407-8-264

Cited by 30 publications

(25 citation statements)

References 30 publications

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“…Other groups have demonstrated that Cdkn1a is regulated by CREB in melanoma cells [57] and myeloid leukemia cells [58], further supporting our results. Notably, our microarray analyses indicated that mRNA levels of Cbp/p300-interacting transactivator 2 (CITED2) were downregulated in CREB mutant mice.…”

Section: Discussionsupporting

confidence: 92%

CREB mediates the insulinotropic and anti-apoptotic effects of GLP-1 signaling in adult mouse β-cells

Shin

Lay

Everett

et al. 2014

Molecular Metabolism

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ObjectiveGlucagon-like peptide-1 (GLP-1) plays a major role in pancreatic β-cell function and survival by increasing cytoplasmic cAMP levels, which are thought to affect transcription through activation of the basic leucine zipper (bZIP) transcription factor CREB. Here, we test CREB function in the adult β-cell through inducible gene deletion.MethodsWe employed cell type-specific and inducible gene ablation to determine CREB function in pancreatic β-cells in mice.ResultsBy ablating CREB acutely in mature β-cells in tamoxifen-treated CrebloxP/loxP;Pdx1-CreERT2 mice, we show that CREB has little impact on β-cell turnover, in contrast to what had been postulated previously. Rather, CREB is required for GLP-1 to elicit its full effects on stimulating glucose-induced insulin secretion and protection from cytokine-induced apoptosis. Mechanistically, we find that CREB regulates expression of the pro-apoptotic gene p21 (Cdkn1a) in β-cells, thus demonstrating that CREB is essential to mediating this critical aspect of GLP-1 receptor signaling.ConclusionsIn sum, our studies using conditional gene deletion put into question current notions about the importance of CREB in regulating β-cell function and mass. However, we reveal an important role for CREB in the β-cell response to GLP-1 receptor signaling, further validating CREB as a therapeutic target for diabetes.

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Section: Discussionsupporting

confidence: 92%

CREB mediates the insulinotropic and anti-apoptotic effects of GLP-1 signaling in adult mouse β-cells

Shin

Lay

Everett

et al. 2014

Molecular Metabolism

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“…S2E). It is also worth mentioning that the sicreb and AD-shcreb targeted different sites on the CREB mRNA, two target sequences that are widely used for silencing CREB (24,26,35,36), which should have reduced the possibility of an off-target effect. In addition, knocking down CREB with AD-shcreb#2 (targeting the same sequence as sicreb) produced similar effects on glioma cell growth, survival and colony formation (Fig.…”

Section: Creb Is Up-regulated In Gliomas and Is Essential For Gliomagmentioning

confidence: 99%

cAMP response element-binding protein promotes gliomagenesis by modulating the expression of oncogenic microRNA-23a

Tan

Wang

Zhu

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

106

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Gliomas are the most common and deadly type of primary brain tumor. In this study, we showed that cAMP response element-binding protein (CREB), a proto-oncogenic transcription factor that is overexpressed in gliomas, can promote gliomagenesis by modulating the expression of oncogenic microRNA-23a (mir-23a). First, we found that CREB is highly expressed in glioma tissues and cell lines. CREB is also essential for glioma cell growth and cell survival in vitro and is critical for gliomagenesis in vivo. Second, microRNA microarray, ChIP-chip, ChIP-quantitative PCR, and luciferase reporter assays showed that CREB directly binds to the regulatory sequences of mir-23a and enhance the expression of mir-23a. Moreover, mir-23a was confirmed as a functional downstream target of CREB in glioma cell growth and cell survival. Finally, using computational prediction followed by experimental confirmation, we identified PTEN, which is frequently silenced in gliomas, as a downstream target of mir-23a. Taken together, we propose that CREB promotes gliomagenesis and acts as a modulator of oncogenic mir-23a, which represses the tumor suppressor PTEN.

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“…In an effort to define the target genes of CREB in leukemias, genome-wide analyses were performed and CREB target genes were described; numerous candidate genes have been identified such as transcription regulators and histones, though these await in vivo validation. 27,28,50 To identify potential downstream target genes, a microarray analysis with RNA from leukemia K562 cells overexpressing CREB was performed. 51 Approximately 896 genes were differentially expressed in the CREB overexpressing cells compared to control parental cells.…”

Section: Creb In Hematopoiesis and Leukemogenesismentioning

confidence: 99%

CREB and Leukemogenesis

2011

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Acute myeloid leukemia (AML) is one of the most common leukemias with a 20% 5-year event-free survival in adults and 50% overall survival in children, despite aggressive chemotherapy treatment and bone marrow transplantation. The incidence and mortality rates for acute leukemia have only slightly decreased over the last 20 years and therefore greater understanding of the molecular mechanisms associated with leukemic progression is needed. To this end, a number of transcription factors which appear to play a central role in leukemogenesis are being investigated; among them is the cAMP response element binding protein (CREB). CREB is a transcription factor that can regulate downstream targets involving in various cellular functions including cell proliferation, survival, and differentiation. In several studies, the majority of bone marrow samples from patients with acute lymphoid and myeloid leukemia demonstrate CREB overexpression. Moreover, CREB overexpression is associated with a poor outcome in AML patients. This review summarizes the role of CREB in leukemogenesis.

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Expression profile of CREB knockdown in myeloid leukemia cells

Cited by 30 publications

References 30 publications

CREB mediates the insulinotropic and anti-apoptotic effects of GLP-1 signaling in adult mouse β-cells

CREB mediates the insulinotropic and anti-apoptotic effects of GLP-1 signaling in adult mouse β-cells

cAMP response element-binding protein promotes gliomagenesis by modulating the expression of oncogenic microRNA-23a

CREB and Leukemogenesis

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