SATB1 overexpression promotes malignant T-cell proliferation in cutaneous CD30+ lymphoproliferative disease by repressing p21

Wei, Xiawei; Gu, Xiaoguang; Zhang, Gaolei; Wang, Lin; Wang, Tingting; Zhao, Yun; Zhang, Xiuyan; Zhou, Youwen; Kadin, Marshall E.; Tu, Ping

doi:10.1182/blood-2013-10-534693

Cited by 32 publications

(41 citation statements)

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“…SATB1 is also involved in rapid induction of multiple cytokines genes on T-helper 2 cell activation22. Recent reports show that SATB1 is correlated with metastatic phenotypes and poor clinical prognosis in various tumors23242526. Consistent with other reports, our former study revealed that SATB1 promoted development and progression of liver cancer by regulation of genes related to cell cycle, apoptosis and EMT2728.…”

supporting

confidence: 87%

Hepatic SATB1 induces paracrine activation of hepatic stellate cells and is upregulated by HBx

Gong

Han

et al. 2016

Sci Rep

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Chronic hepatitis B virus (HBV) infection is a major cause of chronic liver diseases, but its involvement in hepatic fibrogenesis remains unclear. Special AT-rich binding protein 1 (SATB1) has been implicated in reprogramming chromatin organization and transcription profiles in many cancers and non-cancer-related conditions. We found that hepatic SATB1 expression was significantly up-regulated in fibrotic tissues from chronic hepatitis B virus (HBV)-infected patients and HBV transgenic (HBV-Tg) mouse model. Knockdown of SATB1 in the liver significantly alleviated CCl4-induced fibrosis in HBV-Tg mouse model. Moreover, we suggested HBV encoded x protein (HBx) induced SATB1 expression through activation of JNK and ERK pathways. Enforced expression of SATB1 in hepatocytes promoted the activation and proliferation of hepatic stellate cells (HSCs) by secretion of connective tissue growth factor (CTGF), Interleukin-6 (IL-6) and platelet derived growth factor-A (PDGF-AA). Our findings demonstrated that HBx upregulated hepatic SATB1 which exerted pro-fibrotic effects by paracrine activation of stellate cells in HBV-related fibrosis.

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supporting

confidence: 87%

Hepatic SATB1 induces paracrine activation of hepatic stellate cells and is upregulated by HBx

Gong

Han

et al. 2016

Sci Rep

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“…Interestingly, we did not observe increased DNA damage in the senescent cells. However, we found that SATB1 binds directly to the regulatory region of CDKN1A repressing its expression, which is in accordance with previous findings (Wang et al, 2014). Moreover, inhibition of CDKN1A in SATB1 KO DA neurons significantly reduced the number of senescent cells, demonstrating that the direct regulation of p21 levels in SATB1 KO DA neurons triggers the senescence phenotype.…”

Section: Discussionsupporting

confidence: 92%

“…The elimination of SATB1, and the resulting de-repression of CDKN1A, is thus sufficient to elevate cellular p21 levels. In line with these findings, SATB1 has previously been described to regulate cellular senescence in keratinocytes (Lena et al, 2012), and has also been previously described to repress the promoter of CDKN1A (Wang et al, 2014). We next sought to determine the direct role of p21 in inducing the senescent phenotype in SATB1 KO DA neurons.…”

Section: Satb1 Repression Of Cdkn1a Prevents Senescence In Da Neuronsmentioning

confidence: 57%

“…We hypothesize that CDKN1A gene expression in DA neurons is under constant influence of promoting factors which aim to increase cellular p21 levels, whereas in CTX neurons this is not the case. SATB1 is therefore an important repressor of CDKN1A transcription (Wang et al, 2014) and regulates p21 levels in DA neurons.…”

Section: Satb1 Repression Of Cdkn1a Prevents Senescence In Da Neuronsmentioning

confidence: 99%

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Loss of SATB1 Induces a p21 Dependent Cellular Senescence Phenotype in Dopaminergic Neurons

Rießland

Kolisnyk

et al. 2018

Preprint

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Cellular senescence is a mechanism used by mitotic cells to prevent uncontrolled cell division. As senescent cells persist in tissues, they cause local inflammation and are harmful to surrounding cells, contributing to aging. Generally, neurodegenerative diseases, such as Parkinson's, are disorders of aging. The contribution of cellular senescence to neurodegeneration is still unclear. SATB1 is a DNA binding protein associated with Parkinson's disease. We report that SATB1 prevents cellular senescence in post-mitotic dopaminergic neurons. Loss of SATB1 causes activation of a cellular senescence transcriptional program in dopamine neurons, both in human stem cell-derived dopaminergic neurons and in mice. We observed phenotypes which are central to cellular senescence in SATB1 knockout dopamine neurons in vitro and in vivo. Moreover, we found that SATB1 directly represses expression of the pro-senescence factor, p21, in dopaminergic neurons. Our data implicate senescence of dopamine neurons as a contributing factor to the pathology of Parkinson's disease. hESC shows normal appearance. Scale bar: 200 µm. (D) Immunolabeling of DA precursor markers in WT and SATB1 KO hESC derived DA neurons after 16 days of differentiation reveals no difference in marker expression. (E) Depiction of spontaneous action potentials of WT and SATB1 KO DA neurons at different time points show that both genotypes differentiate into mature DA neurons between day 35 and 40. Scale bar: 20 mV, 2 s. (F) DA neurons at day 40 show significant differences in maintenance of response to positive current injections. Scale bar: 20 mV, 200 ms. (G) Longitudinal comparison of cell survival of WT vs. SATB1 KO DA neurons revealed a significant reduction in SATB1 KO survival between day 30 and 40, reaching a plateau at ~50%. Data are represented as mean ± SEM. (H) Quantification of neurite morphology and complexity in WT and SATB1 KO DA neurons. Data are represented as mean ± SEM. (I) Triple immunolabeling of cortical shows that both WT as well as SATB1 KO neurons express the essential markers for cortical neurons. Scale bar: 50 µm. (J) SATB1 KO cortical neurons show no significant change in survival during differentiation. Data are represented as mean ± SEM. (K) Quantification of neurite morphology and complexity in WT and SATB1 KO CTX neurons. (L)Representative western blot and quantification depicts that WT DA neurons express significantly higher levels of SATB1 than WT cortical neurons, suggesting a higher demand in DA neurons. Data are represented as mean ± SEM. See also Figure S1.

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“…Overexpression of this gene has been observed in several types of solid tumors and is positively correlated with prognostic and clinicopathological properties (7). SATB1 is primarily expressed in thymocytes, and regulates the development and maturation of T cells (8,9). Previous studies have demonstrated a correlation between SATB1 expression and the metastasis and poor prognosis of breast cancer (10).…”

Section: Introductionmentioning

confidence: 99%

Effect of SATB1 silencing on the proliferation, invasion and apoptosis of TE-1 esophageal cancer cells

et al. 2017

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The aim of the present study was to investigate the effect of special AT-rich sequence-binding protein-1 (SATB1)-targeted small interfering RNA (siRNA) on the proliferation, invasion and apoptosis of TE-1 human esophageal cancer cells. SATB1 has been correlated with the metastasis and poor prognosis of colon and breast cancer, but the role of SATB1 in esophageal cancer remains unknown. Therefore, the present study constructed and transfected SATB1-siRNA into TE-1 cells in order to knockdown the expression of the SATB1 gene. Western blot analysis, a cell counting kit, transwell chamber assays and flow cytometry were used to assess the effect of SATB1-siRNA on the proliferation, invasion and apoptosis of cells. The results demonstrated that the expression of the SATB1 gene was efficiently knocked down by SATB1-siRNA, and that SATB1-siRNA inhibited the proliferation, invasion and apoptosis of TE-1 cells. Therefore, it was concluded that the SATB1 gene is important in the pathogenesis of human esophageal cancer, and may present a novel therapeutic target for esophageal cancer.

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SATB1 overexpression promotes malignant T-cell proliferation in cutaneous CD30+ lymphoproliferative disease by repressing p21

Abstract: Key Points SATB1 is specifically overexpressed in the CD30+ lymphoma cells in cutaneous CD30+ lymphoproliferative disease. SATB1 promotes proliferation of CD30+ lymphoma cells by direct transcriptional repression of cell cycle inhibitor p21.

Cited by 32 publications

References 50 publications

Hepatic SATB1 induces paracrine activation of hepatic stellate cells and is upregulated by HBx

Hepatic SATB1 induces paracrine activation of hepatic stellate cells and is upregulated by HBx

Loss of SATB1 Induces a p21 Dependent Cellular Senescence Phenotype in Dopaminergic Neurons

Effect of SATB1 silencing on the proliferation, invasion and apoptosis of TE-1 esophageal cancer cells

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