Somatic Single Hits Inactivate the X-Linked Tumor Suppressor FOXP3 in the Prostate

Wang, Lizhong; Liu, Runhua; Li, Weiquan; Chen, Chong; Katoh, Hiroto; Chen, Guo Yun; McNally, Beth A.; Lin, Lin; Zhou, Penghui; Zuo, Tao; Cooney, Kathleen A.; Liu, Yang; Zheng, Pan

doi:10.1016/j.ccr.2009.08.016

Cited by 198 publications

(312 citation statements)

References 54 publications

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“…Evidence for FOXP3 tumour-suppressor function in human epithelial cells is suggested by several studies reporting a high frequency of somatic mutations and deletions of FOXP3 in human breast, ovary and prostate tumour samples (Zuo et al, 2007a, b). Reintroduction of FOXP3 into breast or prostate cancer cell lines results in growth-inhibitory and proapoptotic effects in vitro and in vivo, confirming this causal link (Zhang et al, 2006;Zuo et al, 2007a;Wang et al, 2009).…”

Section: Introductionmentioning

confidence: 49%

“…The transcription factor FOXP3, a master regulator of Treg cells, has been proposed to function as a tumour suppressor in breast and prostate epithelial cells (Zuo et al, 2007b;Wang et al, 2009), although the molecular pathways and the targets it regulates are yet to be explored in detail. In Treg cells, FOXP3 orchestrates its transcriptional programme both by directly binding to gene-regulatory regions and also indirectly by controlling other regulators such as transcription factors and miRs Hill et al, 2007;Williams and Rudensky, 2007;Zheng et al, 2007;Sadlon et al, 2010).…”

Section: Discussionmentioning

confidence: 99%

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FOXP3 and FOXP3-regulated microRNAs suppress SATB1 in breast cancer cells

et al. 2011

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The transcription factor FOXP3 has been identified as a tumour suppressor in the breast and prostate epithelia, but little is known about its specific mechanism of action. We have identified a feed-forward regulatory loop in which FOXP3 suppresses the expression of the oncogene SATB1.In particular, we demonstrate that SATB1 is not only a direct target of FOXP3 repression, but that FOXP3 also induces two miRs, miR-7 and miR-155, which specifically target the 3 0 -UTR of SATB1 to further regulate its expression. We conclude that FOXP3-regulated miRs form part of the mechanism by which FOXP3 prevents the transformation of the healthy breast epithelium to a cancerous phenotype. Approaches aimed at restoring FOXP3 function and the miRs it regulates could help provide new approaches to target breast cancer.

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Section: Introductionmentioning

confidence: 49%

Section: Discussionmentioning

confidence: 99%

FOXP3 and FOXP3-regulated microRNAs suppress SATB1 in breast cancer cells

et al. 2011

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“…Previous studies have reported that Foxp3 is not only expressed in Tregs, but also in tumour cells. Since Hinz et al first reported the expression of Foxp3 in human pancreatic carcinoma cells (5), other studies have shown that Foxp3 is expressed in other tumour cells, including human breast cancer, prostate cancer, lung and melanoma cells (6)(7)(8)(9)(10). In addition, other studies have shown that the expression of Foxp3 within tumour cells is associated with tumour progression and metastasis, and thus it is a poor prognostic factor (5,6).…”

Section: Introductionmentioning

confidence: 99%

Foxp3 expression in A549 cells is regulated by Toll-like receptorï¿½4 through nuclear factor-κB

Yang

2012

Mol Med Report

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Abstract. Foxp3 is a master regulator of the development and function of CD4 + CD25 + regulatory T cells (Tregs). Previous studies have reported that Foxp3 is also expressed in tumour cells and promotes tumour immune evasion. However, the regulation of the expression of Foxp3 in tumour cells remains unclear. Toll-like receptor 4 (TLR4), a member of the pattern recognition receptor family, is also expressed in tumour cells. Previous studies have found that the TLR4 signaling pathway is involved in tumour immune evasion in lung cancer cells, and that the transcription factor, nuclear factor-κB (NF-κB), plays a key role in the TLR4 signaling pathway. Moreover, recent studies found that NF-κB promotes the transcription of Foxp3. We hypothesised that TLR4 may also be involved in the regulation of Foxp3 in A549 cells through NF-κB. Therefore, we examined the effect of TLR4 and NF-κB on the expression of Foxp3 in the A549 lung cancer cell line. The results showed that Foxp3 and TLR4 are expressed in A549 cells; the expression of Foxp3 increased after lipopolysaccharide (LPS) stimulation and decreased after blocking the TLR4 signaling pathway. In addition, the expression of NF-κB (p65) increased after LPS stimulation and the expression of Foxp3 decreased after blocking NF-κB. These results suggest that TLR4 is involved in the regulation of Foxp3 in A549 cells through NF-κB.

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“…The frozen tissues specimens obtained from PTC patients with LNM (n=15) and without LNM (n=10) were used for laser capture microdissection (ArcturusXT™; Thermo Fisher Scientific, Inc., Waltham, MA, USA) to obtain target thyroid epithelial cells, as described previously (34). The age and gender of the participants were matched for each group.…”

Section: Patientsmentioning

confidence: 99%

Pigment epithelium-derived factor has a role in the progression of papillary thyroid carcinoma by affecting the HIF1α-VEGF signaling pathway

Sun

Shi

et al. 2016

Oncology Letters

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Abstract. The progression mechanism of papillary thyroid carcinoma (PTC) remains largely unknown. Accumulating evidence has suggested that various targets of pigment epithelium-derived factor (PEDF) are able to inhibit cancer progression. The aim of the present study was to examine PEDF expression in PTC patients and to investigate its relationship with aggressive clinicopathological features, as well as to explore whether PEDF affects the progression of PTC via the hypoxia-inducible factor 1α (HIF1α)-vascular endothelial growth factor (VEGF) pathway. A total of 271 patients with PTC, including 24 men and 247 women, were enrolled in the present study. Relevant patient data, including demographic features, preoperative clinical features and pathological features, were collected for analysis. The protein expression levels of PEDF in PTC tissues were detected using immunohistochemical staining, and the mRNA expression levels of PEDF, VEGF and HIF1α in 15 PTC tissues with lymph node metastasis (LNM) and 10 tissues without LNM were detected using reverse transcription-quantitative polymerase chain reaction. Immunohistochemical staining with an anti-PEDF antibody detected PEDF expression in 74.5% of the PTC tissues. PEDF expression levels were significantly correlated with LNM, extrathyroid invasion, a high TNM stage, the presence of the BRAF V600E mutation and tumor size. PEDF mRNA expression levels were significantly decreased in PTC tissues with LNM, as compared with PTC tissues without LNM, while the mRNA expression levels of HIF1α and VEGF were markedly increased in PTC tissues with LNM. Taken together, the results of the present study suggested that PEDF plays a role in the progression of PTC, and that PEDF may exert an anti-angiogenesis role by affecting the HIF1α-VEGF pathway, eventually inhibiting the metastasis of PTC.

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Somatic Single Hits Inactivate the X-Linked Tumor Suppressor FOXP3 in the Prostate

Cited by 198 publications

References 54 publications

FOXP3 and FOXP3-regulated microRNAs suppress SATB1 in breast cancer cells

FOXP3 and FOXP3-regulated microRNAs suppress SATB1 in breast cancer cells

Foxp3 expression in A549 cells is regulated by Toll-like receptorï¿½4 through nuclear factor-κB

Pigment epithelium-derived factor has a role in the progression of papillary thyroid carcinoma by affecting the HIF1α-VEGF signaling pathway

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