The protooncogene product, PEBP2β/CBFβ, is mainly located in the cytoplasm and has an affinity with cytoskeletal structures

Tanaka, Yuta; Watanabe, Toshio; Chiba, Natsuko; Niki, Masaru; Kuroiwa, Yasuyuki; Nishihira, Tetsuro; Satoh, Susumu; Ito, Yoshiaki; Satake, Masanobu

doi:10.1038/sj.onc.1201235

Cited by 32 publications

(32 citation statements)

References 23 publications

(33 reference statements)

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“…This might in part explain the discrepancy. Consistent with earlier reports, we found CBFB protein both in the cytoplasm and the nucleus of the neoplastic cells (Tanaka et al, 1997). These locations are in agreement with the known function of CBFB, which constitutes half of the core-binding factor TF complex.…”

Section: Discussionsupporting

confidence: 81%

Dysregulation of the transcription factors SOX4, CBFB and SMARCC1 correlates with outcome of colorectal cancer

et al. 2009

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The aim of this study was to identify deregulated transcription factors (TFs) in colorectal cancer (CRC) and to evaluate their relation with the recurrence of stage II CRC and overall survival. Microarray-based transcript profiles of 20 normal mucosas and 424 CRC samples were used to identify 51 TFs displaying differential transcript levels between normal mucosa and CRC. For a subset of these we provide in vitro evidence that deregulation of the Wnt signalling pathway can lead to the alterations observed in tissues. Furthermore, in two independent cohorts of microsatellite-stable stage II cancers we found that high SOX4 transcript levels correlated with recurrence (HR 2.7; 95% CI, 1.2 -6.0; P ¼ 0.01). Analyses of B1000 stage I -III adenocarcinomas, by immunohistochemistry, revealed that patients with tumours displaying high levels of CBFB and SMARCC1 proteins had a significantly better overall survival rate (P ¼ 0.0001 and P ¼ 0.0275, respectively) than patients with low levels. Multivariate analyses revealed that a high CBFB protein level was an independent predictor of survival. In conclusion, several of the identified TFs seem to be involved in the progression of CRC.

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Section: Discussionsupporting

confidence: 81%

Dysregulation of the transcription factors SOX4, CBFB and SMARCC1 correlates with outcome of colorectal cancer

et al. 2009

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“…59 The majority of CBF␤ is cytoplasmic, likely reflecting its affinity for the actin cytoskeleton and its expression in excess of CBF␣. 59,60 The CBF oncoproteins Chromosomal abnormalities involving subunits of CBF are common in acute leukemias. Inv(16)(p13;q22) or the less common t(16;16)(p13;q22) are present in 10% of acute myeloid leukemia (AML) and encode CBF␤-SMMHC, in which the majority of CBF␤ is fused to the tail domain of a smooth muscle myosin heavy chain (SMMHC).…”

Section: Core Binding Factorsmentioning

confidence: 99%

True

1999

Leukemia

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The AML1 and CBF␤ subunits of core binding factor (CBF) are involved in several chromosomal abnormalities frequently associated with acute leukemias. As a result, the CBF␤-SMMHC, AML1-ETO and AML1-MDS1/EVI1 fusion proteins are expressed in subsets of acute myeloid leukemia, and TEL-AML1 is expressed in B-lineage acute lymphocytic leukemia. These CBF oncoproteins likely contribute to leukemogenesis in part by inhibiting endogenous CBF. As a result they are expected to inhibit differentiation and perhaps apoptosis. In addition, the domains unique to each fusion protein may also contribute to leukemogenesis via unique mechanisms.

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“…These results suggest that CBF regulates the G1 to S transition. However, CBFb interacts with the cytoskeleton (Tanaka et al, 1997) and perhaps other proteins, and the SMMHC domain likely interacts with non-muscle myosins and perhaps other coiled-coil proteins.…”

Section: Introductionmentioning

confidence: 99%

Exogenous cdk4 overcomes reducedcdk4 RNA and inhibition of G1 progression in hematopoietic cells expressing a dominant-negative CBF – a model for overcoming inhibition of proliferation by CBF oncoproteins

Lou¹,

Cao²,

Bernardin³

et al. 2000

Oncogene

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Core Binding Factor (CBF) is required for the development of de®nitive hematopoiesis, and the CBF oncoproteins AML1-ETO, TEL-AML1, and CBFb-SMMHC are commonly expressed in subsets of acute leukemia. CBFb-SMMHC slows the G1 to S cell cycle transition in hematopoietic cells, but the mechanism of this e ect is uncertain. We have sought to determine whether inhibition of CBF-mediated trans-activation is su cient to slow proliferation. We demonstrate that activation of KRAB-AML1-ER, a protein containing the AML1 DNA-binding domain, the KRAB repression domain, and the Estrogen receptor ligand binding domain, also slows G1, if its DNA-binding domain is intact. Also, exogenous AML1 overcame CBFb-SMMHC-induced inhibition of proliferation. Representational di erence analysis (RDA) identi®ed cdk4 RNA expression as an early target of KRAB-AML1 activation. Inhibition of CBF activities by KRAB-AML1-ER or CBFb-SMMHC rapidly reduced endogenous cdk4 mRNA levels, even in cells proliferating at or near control rates as a result of exogenous cdk4 expression. Over-expression of cdk4, especially a variant which cannot bind p16 INK4a , overcame cell cycle inhibition resulting from activation of KRAB-AML1-ER, although cdk4 did not accelerate proliferation when expressed alone. These ®ndings indicate that mutations which alter the expression of G1 regulatory proteins can overcome inhibition of proliferation by CBF oncoproteins.

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The protooncogene product, PEBP2β/CBFβ, is mainly located in the cytoplasm and has an affinity with cytoskeletal structures

Cited by 32 publications

References 23 publications

Dysregulation of the transcription factors SOX4, CBFB and SMARCC1 correlates with outcome of colorectal cancer

Dysregulation of the transcription factors SOX4, CBFB and SMARCC1 correlates with outcome of colorectal cancer

True

Exogenous cdk4 overcomes reducedcdk4 RNA and inhibition of G1 progression in hematopoietic cells expressing a dominant-negative CBF – a model for overcoming inhibition of proliferation by CBF oncoproteins

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