Deficiency of SATB1 expression in Sézary cells causes apoptosis resistance by regulating FasL/CD95L transcription

Wang, Yang; Su, Mingwan; Zhou, Liang; Tu, Ping; Zhang, Xuejun; Jiang, Xiaoyan; Zhou, Youwen

doi:10.1182/blood-2010-07-294819

Cited by 56 publications

(95 citation statements)

References 49 publications

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“…Notably, VCR-induced apoptosis was largely eliminated by SATB1 overexpression in SGC7901 cells. These results are consistent with previous studies which revealed that SATB1 inhibited apoptosis in Sézary and breast cancer cells (14,23), suggesting that the SATB1-mediated inhibition of apoptosis may contribute to MDR in gastric cancer.…”

Section: Discussionsupporting

confidence: 83%

Special AT-rich sequence binding protein 1 regulates the multidrug resistance and invasion of human gastric cancer cells

Sun

et al. 2012

Oncology Letters

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Abstract. Special AT-rich sequence binding protein 1 (SATB1) is a nuclear factor that functions as a global chromatin organizer to regulate gene expression. Recent studies have suggested an oncogenic role of SATB1 in breast cancer. However, the role of SATB1 in gastric cancer, especially in regulating the malignant phenotypes, including multidrug resistance (MDR) and metastasis, remains poorly understood. In this study, the aggressive human gastric cancer cell line SGC7901 and its corresponding MDR variant SGC7901/VCR cells were used as a model. SATB1 expression was examined by RT-PCR and western blot analysis. Results showed that SATB1 was upregulated in SGC7901/VCR cells. An in vitro drug sensitivity assay demonstrated a positive correlation between SATB1 expression levels and drug resistance. Gain and loss of SATB1 function experiments further demonstrated that SATB1 contributes to MDR by inhibiting the accumulation of vincristine (VCR) in gastric cancer cells and protecting the cells from VCR-induced apoptosis. In addition, SATB1 may promote the invasion of gastric cancer cells. The present study provides a novel insight into the oncogenic role of SATB1 in gastric cancer, suggesting that SATB1 is a promising target for the therapy of drug-resistant and invasive gastric cancer.

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Section: Discussionsupporting

confidence: 83%

Special AT-rich sequence binding protein 1 regulates the multidrug resistance and invasion of human gastric cancer cells

Sun

et al. 2012

Oncology Letters

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“…Downregulation of SATB1 in Jurkat cells caused their resistance to induced cell death [40]. In line with these observations, Wang et al reported that deficiency in SATB1 expression in Sézary cells caused resistance to apoptosis [41]. However, Chu et al found that downregulation of SATB1 expression was responsible for the initiation of active cell death [42].…”

supporting

confidence: 58%

The interactions between SATB1 and F-actin are important for mechanisms of active cell death

Grzanka

Kowalczyk²,

Izdebska³

et al. 2015

Folia Histochem Cytobiol.

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Introduction. The direct involvement of nuclear actin filaments in gene transcription and remodeling of chromatin is still debatable. However, nuclear localization of F-actin and its interactions with other nuclear matrix proteins have been reported. The aim of the study was to estimate the interactions between nuclear F-actin and one of the matrix proteins, special AT-rich sequence-binding protein 1 (SATB1), during active cell death induced in vitro by geldanamycin (GA). Material and methods. The expression of SATB1 was modified by the transfection of non-aggressive breast cancer MCF-7 cells with siRNA against SATB1 or expression plasmid with cloned cDNA of SATB1. The amount and localization of F-actin were altered by changes of cofilin-1 (CFL1) expression in MCF-7 cells. The association between SATB1 and F-actin during GA-induced cell death was analyzed using confocal and transmission electron microscopy. Results. Our studies revealed the colocalization between nuclear F-actin and SATB1 protein, during GA-induced death of breast cancer MCF-7 cells. The colocalization was enhanced in cells with overexpressed SATB1 and cofilin-1. At the ultrastructural level the SATB1 and F-actin complexes were seen at the border of condensed and decondensed chromatin. The presence of SATB1/F-actin molecular complexes was confirmed by magnetic separation of F-actin and interacting proteins. Conclusion. We suggest that the molecular interactions between SATB1 and F-actin are necessary for active cell death to occur.

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“…The transcriptome analysis of these SATB1 restored cells showed remarkable up-regulation of FASL/CD95L which is a death receptor ligand. Further, 32 out of total 153 (12%) dysregulated genes in Sézary cells were normalized upon SATB1 restoration in these cells (Wang et al, 2011). The increased AICD in SATB1 restored Sézary cells was shown to be induced by FASL via caspase 8-dependent pathway.…”

Section: Loss Of Satb1 Function: Sézary Syndromementioning

confidence: 92%

“…Transcription profiling of the Sézary cells from patients and Hut78 (Sézary-derived cell line) revealed that SATB1 was drastically downregulated in these cells as compared to non-Sézary control cells such as Jurkat T cells. Additionally, immunofluorescence staining showed a lowered nuclear localization of SATB1 in of primary Sézary cells as well as in Hut98 cells (Wang et al, 2011). Retroviral transduction mediated restoration of SATB1 in Hut98 cells increased apoptosis in these cells within 4 days without changing their proliferation rate.…”

Section: Loss Of Satb1 Function: Sézary Syndromementioning

confidence: 99%

See 1 more Smart Citation

SATB1: Key Regulator of T Cell Development and Differentiation

Gottimukkala¹,

Burute²,

Galande³

2012

Hematology - Science and Practice

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Deficiency of SATB1 expression in Sézary cells causes apoptosis resistance by regulating FasL/CD95L transcription

Cited by 56 publications

References 49 publications

Special AT-rich sequence binding protein 1 regulates the multidrug resistance and invasion of human gastric cancer cells

Special AT-rich sequence binding protein 1 regulates the multidrug resistance and invasion of human gastric cancer cells

The interactions between SATB1 and F-actin are important for mechanisms of active cell death

SATB1: Key Regulator of T Cell Development and Differentiation

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