Expression of Chicken Ovalbumin Upstream Promoter-Transcription Factor II Enhances Invasiveness of Human Lung Carcinoma Cells

Navab, Roya; Gonzalez-Santos, Juana Maria; Johnston, Michael; Jiang, Liu; Brodt, Pnina; Tsao, Ming‐Sound; Hu, Jim

doi:10.1158/0008-5472.can-03-1185

Cited by 39 publications

(38 citation statements)

References 47 publications

(42 reference statements)

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“…Reprobing with Src-specific antibody confirmed that the 60-kDa band represented the phosphorylated pp60 c-Src protein. To investigate the functional relationship between Src and Id1 and its therapeutic implications, we examined a panel of human cancer cell lines from four types of cancer, including lung (A549 and H460), breast (T47D and MDA-MB231), prostate (LNCaP and PC-3), and colon (HCT-116 and HT-29), each represented by a pair of cell lines with different invasive potential (36)(37)(38)(39). Protein extracts of cells grown under normal conditions were subjected to Western blotting for pY419-Src, total Src, Id1, and actin (Fig.…”

Section: Resultsmentioning

confidence: 99%

Regulation of Id1 Expression by Src: Implications for Targeting of the Bone Morphogenetic Protein Pathway in Cancer

et al. 2008

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Deregulated activation of the Src tyrosine kinase and heightened Id1 expression are independent mediators of aggressive tumor biology. The present report implicates Src signaling as a critical regulator of Id1 gene expression. Microarray analyses showed that Id family genes were among the most highly down-regulated by incubation of A549 lung carcinoma cells with the small-molecule Src inhibitor AZD0530. Id1 transcript and protein levels were potently reduced in a dose-dependent manner concomitantly with the reduction of activated Src levels. These effects were conserved across a panel of lung, breast, prostate, and colon cancer cell lines and confirmed by the ability of PP2, Src siRNA, and Srcblocking peptides to suppress Id1 expression. PP2, AZD0530, and dominant-negative Src abrogated Id1 promoter activity, which was induced by constitutively active Src. The Srcresponsive region of the Id1 promoter was mapped to a region 1,199 to 1,360 bps upstream of the translation start site and contained a Smad-binding element. Src was also required for bone morphogenetic protein-2 (BMP-2)-induced Id1 expression and promoter activity, was moderately activated by BMP-2, and complexed with Smad1/5. Conversely, Src inhibitors blocked Smad1/5 nuclear translocation and binding to the Src-responsive region of the Id1 promoter. Consistent with a role for Src and Id1 in cancer cell invasion, Src inhibitors and Id1 siRNA decreased cancer cell invasion, which was increased by Id1 overexpression. Taken together, these results reveal that Src positively interacts with the BMP-Smad-Id pathway and provide new ways for targeted inhibition of Id1. [Cancer Res 2008;68(7):2250-8]

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Section: Resultsmentioning

confidence: 99%

Regulation of Id1 Expression by Src: Implications for Targeting of the Bone Morphogenetic Protein Pathway in Cancer

et al. 2008

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“…CXCL12 expression in primary tumors has recently been reported to drive breast cancer metastasis (Ray et al 2015). The other COUP-TF member, COUP-TF2, may also have a role in breast cancer cell migration and invasion with a report that transfection of COUP-TF2 into MDA-MB-231 resulted in increased migration and invasion of these cells (Navab et al 2004). Together these findings suggest a potential involvement of COUP-TFs in epithelialto-mesenchymal transition and migration of breast cancer cells.…”

Section: Estrogen-relatedmentioning

confidence: 92%

Emerging functional roles of nuclear receptors in breast cancer

Doan

Graham

2017

Journal of Molecular Endocrinology

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Nuclear receptors (NRs) have been targets of intensive drug development for decades due to their roles as key regulators of multiple developmental, physiological and disease processes. In breast cancer, expression of the estrogen and progesterone receptor remains clinically important in predicting prognosis and determining therapeutic strategies. More recently, there is growing evidence supporting the involvement of multiple nuclear receptors other than the estrogen and progesterone receptors, in the regulation of various processes important to the initiation and progression of breast cancer. We review new insights into the mechanisms of action of NRs made possible by recent advances in genomic technologies and focus on the emerging functional roles of NRs in breast cancer biology, including their involvement in circadian regulation, metabolic reprogramming and breast cancer migration and metastasis.

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“…Expression of COUP-TFII in human lung carcinoma cell lines was reported to increase invasive and migratory abilities (39). To examine whether COUP-TFII expression correlates with the invasiveness of human breast cancer cells, we examined in vitro cell invasiveness and migration in vector-transfected versus the LY2-COUP-TFII cell line.…”

Section: Cancer Researchmentioning

confidence: 99%

Decreased Chicken Ovalbumin Upstream Promoter Transcription Factor II Expression in Tamoxifen-Resistant Breast Cancer Cells

Riggs

Wickramasinghe²,

Cochrum³

et al. 2006

Cancer Research

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Tamoxifen (TAM) is successfully used for the treatment and prevention of breast cancer. However, many patients that are initially TAM responsive develop tumors that are antiestrogen/TAM resistant (TAM-R). The mechanism behind TAM resistance in estrogen receptor A (ERA)-positive tumors is not understood. The orphan nuclear receptor chicken ovalbumin upstream promoter transcription factor (COUP-TF)-I interacts directly with 4-hydroxytamoxifen (4-OHT)-and estradiol (E 2 )-occupied ERA, corepressors NCoR and SMRT, and inhibit E 2 -induced gene transcription in breast cancer cells. Here we tested the hypothesis that reduced COUP-TFI and COUP-TFII correlate with TAM resistance. We report for the first time that COUP-TFII, but not COUP-TFI, is reduced in three antiestrogen/TAM-R cell lines derived from TAMsensitive (TAM-S) MCF-7 human breast cancer cells and in MDA-MB-231 cells compared with MCF-7. ERA and ERB protein expression was not different between TAM-S and TAM-R cells, but progesterone receptor (PR) was decreased in TAM-R cells. Further, E 2 increased COUP-TFII transcription in MCF-7, but not TAM-R, cells. Importantly, reexpression of COUP-TFII in TAM-S cells to levels comparable to those in MCF-7 was shown to increase 4-OHT-mediated growth inhibition and increased apoptosis. Conversely, knockdown of COUP-TFII in TAM-S MCF-7 cells blocked growth inhibitory activity and increased 4-OHT agonist activity. 4-OHT increased COUP-TFII-ERA interaction f2-fold in MCF-7 cells. COUP-TFII expression in TAM-R cells also inhibited 4-OHT-induced endogenous PR and pS2 mRNA expression. These data indicate that reduced COUP-TFII expression correlates with acquired TAM resistance in human breast cancer cell lines and that COUP-TFII plays a role in regulating the growth inhibitory activity of TAM in breast cancer cells.

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Expression of Chicken Ovalbumin Upstream Promoter-Transcription Factor II Enhances Invasiveness of Human Lung Carcinoma Cells

Cited by 39 publications

References 47 publications

Regulation of Id1 Expression by Src: Implications for Targeting of the Bone Morphogenetic Protein Pathway in Cancer

Regulation of Id1 Expression by Src: Implications for Targeting of the Bone Morphogenetic Protein Pathway in Cancer

Emerging functional roles of nuclear receptors in breast cancer

Decreased Chicken Ovalbumin Upstream Promoter Transcription Factor II Expression in Tamoxifen-Resistant Breast Cancer Cells

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