Upregulation of SATB1 is associated with the development and progression of glioma

Chu, Sheng-Hua; Ma, Yupo; Feng, Donghan; Zhang, Hong; Zhu, Zhenan; Li, Zhiqiang; Jiang, Pu-cha

doi:10.1186/1479-5876-10-149

Cited by 54 publications

(64 citation statements)

References 35 publications

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“…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: 51%

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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supporting

confidence: 51%

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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“…Epigenetic modifications and dynamic changes in chromatin organization by organizer proteins have recently been shown to play an instrumental role in regulating cancer-promoting genes [34,35]. Aberrant expression of SATB1 mRNA and protein has been shown to promote growth and metastasis of various neoplasms [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26]. The main and most quoted role of SATB1 is chromatin organization and functioning as a global regulator of gene expression, among others during cancer development (e.g.…”

Section: Discussionmentioning

confidence: 99%

“…SATB1 as a MAR-binding protein regulates the genes by folding chromatin into loop domain [8]. It was found to regulate gene expression in thymocytes and pre B-cells [9], but recent studies have shown that SATB1 promotes tumor growth and metastasis through chromatin gene recombination in many neoplasms such as breast, gastrointestinal tract (predominantly colorectal region), liver, laryngeal, lung, thyroid, urinary bladder, ovarian and prostate cancers, melanomas, osteosarcomas, gliomas and some types of leukemias [10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25][26]. Furthermore, except SATB1 involvement in tumor progression by its mRNA and protein overexpression in some cancers, e.g.…”

Section: Introductionmentioning

confidence: 99%

Expression of SATB1 protein in the ductal breast carcinoma tissue microarrays — preliminary study

Kobierzycki

Wojnar²,

Dzięgiel³

2014

Folia Histochem Cytobiol.

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Special AT-rich sequence-binding protein 1 (SATB1) is a nuclear matrix protein which interacts with specific regions of DNA, ensuring its proper organization and function in the cell. The expression of SATB1 was primarily found in thymocytes, but its increased levels were observed in various types of cancers. However, the knowledge of the function and application possibilities of this protein is still limited. The aim of this study was to investigate the expression of SATB1 protein using immunohistochemistry and tissue microarray (TMA) technique and determine its possible relationship with the proliferative marker Ki-67, estrogen a (ER) and progesterone (PR) receptors as well as grade of histological malignancy (G). The study was performed on material of 48 archival invasive ductal breast cancers (IDC). The TMAs were prepared with the use of 0.6 mm diameter punches. Immunohistochemical reactions were carried out using antibodies against Ki-67, ER, PR and SATB1 proteins. The intensity of the nuclear reaction was evaluated using a light microscope and computer-assisted image analysis. Expression of Ki-67 and SATB1 protein was observed in 89.58% and 31.25% of cancer cases, respectively. 62.5% of tumors were classified as ER-positive, and 47.92% as PR-positive. Statistical analysis showed a moderate positive correlation between Ki-67 and SATB1 expression (r = 0.291, p = 0.045 independently on the receptor status, and r = 0.392, p = 0.032 in ER-negative tumors). The expression of the Ki-67 antigen increased with higher grade of histological malignancy (G). The results suggest that SATB1 protein may play an indirect role in the cell proliferation and should be evaluated in relation to the other markers. Further studies concerning determination of its role in cancer progression and metastasis, in terms of application as therapeutic target and prognostic marker, are recommended.

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“…8 The role of SATB1 in development of multiple cancers has been extensively studied. 7 Aberrant SATB1 expression has been shown to be associated with multiple cancers including liver cancer, 9 ovarian cancer, 10 Glioma, 11 gastric cancer. 12,13 Recently, potential role of SATB1 in colorectal cancer development has been studied.…”

Section: Introductionmentioning

confidence: 99%

Wnt/β-catenin signaling regulated SATB1 promotes colorectal cancer tumorigenesis and progression

et al. 2015

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The chromatin organizer SATB1 has been implicated in the development and progression of multiple cancers including breast and colorectal cancers. However, the regulation and role of SATB1 in colorectal cancers is poorly understood. Here, we demonstrate that expression of SATB1 is induced upon hyperactivation of Wnt/β-catenin signaling and repressed upon depletion of TCF7L2 (TCF4) and β-catenin. Using several colorectal cancer cell line models and the APC min mutant zebrafish in vivo model, we established that SATB1 is a novel target of Wnt/β-catenin signaling. We show that direct binding of TCF7L2/β-catenin complex on Satb1 promoter is required for the regulation of SATB1. Moreover, SATB1 is sufficient to regulate the expression of β-catenin, members of TCF family, multiple downstream effectors and mediators of Wnt pathway. SATB1 potentiates the cellular changes and expression of key cancer-associated genes in non-aggressive colorectal cells, promotes their aggressive phenotype and tumorigenesis in vivo. Conversely, depletion of SATB1 from aggressive cells reprograms the expression of cancer-associated genes, reverses their cancer phenotype and reduces the potential of these cells to develop tumors in vivo. We also show that SATB1 and β-catenin bind to the promoters of TCF7L2 and the downstream targets of Wnt signaling and regulate their expression. Our findings suggest that SATB1 shares a feedback regulatory network with TCF7L2/β-catenin signaling and is required for Wnt signaling-dependent regulation of β-catenin. Collectively, these results provide unequivocal evidence to establish that SATB1 reprograms the expression of tumor growth- and metastasis-associated genes to promote tumorigenesis and functionally overlaps with Wnt signaling critical for colorectal cancer tumorigenesis.

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Upregulation of SATB1 is associated with the development and progression of glioma

Cited by 54 publications

References 35 publications

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

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

Expression of SATB1 protein in the ductal breast carcinoma tissue microarrays — preliminary study

Wnt/β-catenin signaling regulated SATB1 promotes colorectal cancer tumorigenesis and progression

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