Activation of B‐Myb by E2F1 in hepatocellular carcinoma

Nakajima, Tomoaki; Yasui, Kohichiroh; Zen, Keika; Inagaki, Yoshikazu; Fujii, Hideki; Minami, Masahito; Tanaka, Shinji; Taniwaki, Masafumi; Itoh, Yoshito; Arii, Shigeki; Inazawa, Johji; Okanoue, Takeshi

doi:10.1111/j.1872-034x.2008.00324.x

Cited by 58 publications

(59 citation statements)

References 30 publications

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“…In agreement with previous data obtained in other cell models (36)(37)(38), our present findings also suggested that E2F1 is involved in B-Myb downregulation at transcriptional level. First of all, we could show that the modulation of mRNA levels of E2F1 and B-Myb transcription factors, assessed in response to Nutlin-3 in all cell types investigated, significantly and positively correlated.…”

Section: Discussionsupporting

confidence: 83%

“…By computational analysis (as predicted by SABiosciences' Text Mining Application and the UCSC Genome Browser) both E2F1 and B-Myb promoters exhibit several p53 consensus DNA binding sites, which have previously suggested a gene regulation/repression occurring through p53 binding directly to the consensus DNA binding sequences (36,37). In addition, E2F1 DNA binding sites have been found in the B-Myb regulatory region, indicating that a potential regulation of B-Myb is also mediated by E2F1 (36)(37)(38).…”

Section: Transcriptional Downregulation Of B-myb and E2f1mentioning

confidence: 99%

“…In addition, E2F1 DNA binding sites have been found in the B-Myb regulatory region, indicating that a potential regulation of B-Myb is also mediated by E2F1 (36)(37)(38). This was confirmed in our cell model by E2F1 knockdown experiments.…”

Section: Transcriptional Downregulation Of B-myb and E2f1mentioning

confidence: 99%

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miR-34a Induces the Downregulation of BothE2F1andB-MybOncogenes in Leukemic Cells

Zauli

Voltan

Iasio

et al. 2011

Clinical Cancer Research

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Purpose: To elucidate new molecular mechanisms able to downregulate the mRNA levels of key oncogenes, such as B-Myb and E2F1, in a therapeutic perspective.Experimental Design: B-Myb and E2F1 mRNA levels were evaluated in primary B chronic lymphocytic leukemia (B-CLL, n ¼ 10) and acute myeloid leukemia (AML, n ¼ 5) patient cells, in a variety of p53 Conclusions: Owing to the role of B-Myb and E2F1 transcription factors in controlling cell-cycle progression of leukemic cells, the downregulation of these oncogenes by miR-34a suggests the usefulness of therapeutic approaches aimed to modulate the levels of miR-34a. Clin Cancer Res; 17(9); 2712-24. Ó2011 AACR.

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Section: Discussionsupporting

confidence: 83%

Section: Transcriptional Downregulation Of B-myb and E2f1mentioning

confidence: 99%

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miR-34a Induces the Downregulation of BothE2F1andB-MybOncogenes in Leukemic Cells

Zauli

Voltan

Iasio

et al. 2011

Clinical Cancer Research

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“…Studies have reported that MYBL2 overexpression in different tumours, including HCC [18, 22, 23], and MYBL2 has been implicated in the progression of breast cancer and colorectal cancer [19, 20, 24]. However, the expression and biological function of MYBL2 in GBC have not been previously investigated.…”

Section: Discussionmentioning

confidence: 99%

MYBL2 is a Potential Prognostic Marker that Promotes Cell Proliferation in Gallbladder Cancer

Liang

Yang²,

Ma³

et al. 2017

Cell Physiol Biochem

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Background: Gallbladder cancer (GBC) is an aggressive and highly lethal biliary tract malignancy, with extremely poor prognosis. In the present study, we analyzed the potential involvement of MYBL2, a member of the Myb transcription factor family, in the carcinogenesis of human GBC. Methods: MYBL2 expression levels were measured in GBC and cholecystitis tissue specimens using quantitative real-time PCR (qRT-PCR) and immunohistochemical (IHC) assays. The effects of MYBL2 on cell proliferation and DNA synthesis were evaluated using Cell Counting Kit-8 assay (CCK-8), colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) retention assay, flow cytometry analysis, western blot, and a xenograft model of GBC cells in nude mice. Results: MYBL2 expression was increased in GBC tissues and associated with histological differentiation, tumour invasion, clinical stage and unfavourable overall survival in GBC patients. The downregulation of MYBL2 expression resulted in the inhibition of GBC cell proliferation, and DNA replication in vitro, and the growth of xenografted tumours in nude mice. Conversely, MYBL2 overexpression resulted in the opposite effects. Conclusions: MYBL2 overexpression promotes GBC cell proliferation through the regulation of the cell cycle at the S and G2/M phase transitions. Thus, MYBL2 could serve as a potential prognostic and therapeutic biomarker in GBC patients.

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“…Aberrant B-MYB expression or amplification has been documented in different types of human cancers, suggesting a role in tumorigenesis [33][34][35]. Furthermore B-MYB was recently implicated in the maintenance of pluripotency, chromatin stability and normal cell cycle progression [36][37][38].…”

Section: Discussionmentioning

confidence: 99%

Addiction of MYCN Amplified Tumours to B-MYB Underscores a Reciprocal Regulatory Loop

Gualdrini¹,

Corvetta²,

Cantilena³

et al. 2010

Oncotarget

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Activation of B‐Myb by E2F1 in hepatocellular carcinoma

Abstract: MYBL2 is a probable transcriptional target of E2F1 in HCC and may therefore be a useful biomarker for diagnosis and an attractive target for molecular therapies useful to treat HCC.

Cited by 58 publications

References 30 publications

miR-34a Induces the Downregulation of BothE2F1andB-MybOncogenes in Leukemic Cells

miR-34a Induces the Downregulation of BothE2F1andB-MybOncogenes in Leukemic Cells

MYBL2 is a Potential Prognostic Marker that Promotes Cell Proliferation in Gallbladder Cancer

Addiction of MYCN Amplified Tumours to B-MYB Underscores a Reciprocal Regulatory Loop

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