Nuclear overexpression of the E2F3 transcription factor in human lung cancer

Cooper, Christopher S.; Nicholson, Andrew G.; Foster, Christopher S.; Dodson, Andrew; Edwards, Sandra E.; Fletcher, A.; Roe, Toby; Clark, Jeremy; Joshi, Anupam; Norman, A.; Feber, Andrew; Lin, Dongmei; Gao, Yanning; Shipley, Janet; Cheng, Shujun

doi:10.1016/j.lungcan.2006.07.005

Cited by 80 publications

(75 citation statements)

References 19 publications

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“…It is still a matter of debate what role, if any, the RB/E2F pathway plays in the development of CRC (Hildebrandt et al, 2000;Nevins, 2001). Consistent with earlier studies not finding E2F3 in normal lung, bladder and prostate tissue Foster et al, 2004;Cooper et al, 2006) we found that E2F3 was generally not expressed by the normal colon epithelia. In contrast, our analysis of CRC specimens showed high E2F3 transcript and protein levels, and revealed a dramatic reduction in the RB1/E2F3 transcript ratio.…”

Section: Discussionsupporting

confidence: 90%

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: 90%

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

et al. 2009

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“…The importance of Aurora-A and E2F3 in oncogenesis has been well established by their alterations in human neoplasms and their capacity to induce cell transformation (27)(28)(29)40). Based on our current observations, we believe that Aurora-A, as a mitotic E2F3 target gene, could mediate E2F3 oncogenic function.…”

Section: Discussionsupporting

confidence: 64%

“…ϳl5%), suggesting the mechanism of activating transcription and/or translation of Aurora-A in ovarian cancer cells. Although overexpression of E2F3 has been detected in different tumors (27)(28)(29), the E2F3 status in ovarian cancer has not been well documented. Thus, we reasoned that E2F3 could be elevated in ovarian cancer and might be a causal factor of up-regulation of Aurora-A.…”

Section: E2f3 Binds To Andmentioning

confidence: 99%

Identification of Aurora-A as a Direct Target of E2F3 during G2/M Cell Cycle Progression

Yang

et al. 2008

Journal of Biological Chemistry

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. Further, E2F3 directly binds to Aurora-A promoter and stimulates the promoter activity. Deletion and mutation analyses of the Aurora-A promoter revealed that a region located 96-bp upstream of the transcription initiation site is critical for the activation of the promoter by E2F3. In addition, expression of E2F3 positively correlates with the protein level of Aurora-A in human ovarian cancer examined. These results indicate for the first time that Aurora-A is transcriptionally regulated by E2F3 during the cell cycle and that E2F3 is a causal factor for up-regulation of Aurora-A in a subset of human ovarian cancer. Thus, the E2F3-Aurora-A axis could be an important target for cancer intervention.

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“…Amplification and overexpression of E2F3 is found in lung, bladder, prostate and ovarian cancers. [3][4][5][6] The E2F3 locus encodes two isoforms: E2F3A and E2F3B, which are distinguished exclusively by their N termini. [7][8][9] Two distinct promoters control the expression of alternative first exons that are spliced to a common second exon.…”

Section: Introductionmentioning

confidence: 99%

APC/C^Cdh1controls the proteasome-mediated degradation of E2F3 during cell cycle exit

et al. 2012

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Nuclear overexpression of the E2F3 transcription factor in human lung cancer

Cited by 80 publications

References 19 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

Identification of Aurora-A as a Direct Target of E2F3 during G2/M Cell Cycle Progression

APC/C^Cdh1controls the proteasome-mediated degradation of E2F3 during cell cycle exit

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Nuclear overexpression of the E2F3 transcription factor in human lung cancer

Cited by 80 publications

References 19 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

Identification of Aurora-A as a Direct Target of E2F3 during G2/M Cell Cycle Progression

APC/CCdh1controls the proteasome-mediated degradation of E2F3 during cell cycle exit

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APC/C^Cdh1controls the proteasome-mediated degradation of E2F3 during cell cycle exit