The Experts below are selected from a list of 7386 Experts worldwide ranked by ideXlab platform
Sanjeev Galande - One of the best experts on this subject based on the ideXlab platform.
-
SATB family chromatin organizers as master regulators of tumor progression
Oncogene, 2019Co-Authors: Rutika Naik, Sanjeev GalandeAbstract:SATB (Special AT-rich binding protein) family proteins have emerged as key regulators that integrate higher-order chromatin organization with the regulation of gene expression. Studies over the past decade have elucidated the specific roles of SATB1 and SATB2, two closely related members of this family, in cancer progression. SATB family chromatin organizers play diverse and important roles in regulating the dynamic equilibrium of apoptosis, cell invasion, metastasis, proliferation, angiogenesis, and immune modulation. This review highlights cellular and molecular events governed by SATB1 influencing the structural organization of chromatin and interacting with several co-activators and co-repressors of transcription towards tumor progression. SATB1 expression across tumor cell types generates cellular and molecular heterogeneity culminating in tumor relapse and metastasis. SATB1 exhibits dynamic expression within intratumoral cell types regulated by the tumor microenvironment, which culminates towards tumor progression. Recent studies suggested that cell-specific expression of SATB1 across tumor recruited dendritic cells (DC), cytotoxic T lymphocytes (CTL), T regulatory cells (Tregs) and tumor epithelial cells along with tumor microenvironment act as primary determinants of tumor progression and tumor inflammation. In contrast, SATB2 is differentially expressed in an array of cancer types and is involved in tumorigenesis. Survival analysis for patients across an array of cancer types correlated with expression of SATB family chromatin organizers suggested tissue-specific expression of SATB1 and SATB2 contributing to disease prognosis. In this context, it is pertinent to understand molecular players, cellular pathways, genetic and epigenetic mechanisms governed by cell types within tumors regulated by SATB proteins. We propose that patient survival analysis based on the expression profile of SATB chromatin organizers would facilitate their unequivocal establishment as prognostic markers and therapeutic targets for cancer therapy.
-
wnt β catenin signaling regulated SATB1 promotes colorectal cancer tumorigenesis and progression
Oncogene, 2016Co-Authors: Rafeeq Mir, Saurabh J. Pradhan, Prithviraj Patil, R. Mulherkar, Sanjeev GalandeAbstract: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.
-
Wnt/β-catenin signaling regulated SATB1 promotes colorectal cancer tumorigenesis and progression.
Oncogene, 2015Co-Authors: Rafeeq Mir, Saurabh J. Pradhan, Prithviraj Patil, R. Mulherkar, Sanjeev GalandeAbstract: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.
-
Wnt/β-catenin signaling regulated SATB1 promotes colorectal cancer
2015Co-Authors: Rafeeq Mir, Saurabh J. Pradhan, Prithviraj Patil, R. Mulherkar, Sanjeev GalandeAbstract: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.
-
Acetylation-dependent interaction of SATB1 and CtBP1 mediates transcriptional repression by SATB1.
Molecular and cellular biology, 2008Co-Authors: Prabhat Kumar Purbey, Sunita Singh, Dimple Notani, Pankaj Kumar, Amita Limaye, Sanjeev GalandeAbstract:Special AT-rich binding protein 1 (SATB1) acts as a global regulator of gene expression by recruiting various corepressor or coactivator complexes, thereby establishing a unique chromatin structure at its genomic targets in a context-dependent manner. Although SATB1 acts predominantly as a repressor via recruitment of histone deacetylase 1 (HDAC1) complexes, the precise mechanism of global repression is not clear. Here we report that SATB1 and C-terminal binding protein 1 (CtBP1) form a repressor complex in vivo. The interaction occurs via the CtBP1 interaction consensus motif PVPLS within the PDZ-like domain of SATB1. The acetylation of SATB1 upon LiCl and ionomycin treatments disrupts its association with CtBP1, resulting in enhanced target gene expression. Chromatin immunoprecipitation analysis indicated that the occupancy of CtBP1 and HDAC1 is gradually decreased and the occupancy of PCAF is elevated at the SATB1 binding sites within the human interleukin-2 and mouse c-Myc promoters. Moreover, gene expression profiling studies using cells in which expression of SATB1 and CtBP1 was silenced indicated commonly targeted genes that may be coordinately repressed by the SATB1-CtBP1 complex. Collectively, these results provide a mechanistic insight into the role of SATB1-CtBP1 interaction in the repression and derepression of SATB1 target genes during Wnt signaling in T cells.
Zhiliang Liu - One of the best experts on this subject based on the ideXlab platform.
-
silencing SATB1 with sirna inhibits the proliferation and invasion of small cell lung cancer cells
Cancer Cell International, 2013Co-Authors: Bo Huang, Xiaodong Wang, Hongli Zhou, Zhiliang LiuAbstract:Background: Small cell lung cancer (SCLC) is a special kind of lung cancers, lymph or blood metastasis of SCLC usually occurs in early stage. Studies in breast and colon cancer showed over expression of SATB1 could promote tumor cell growth and inhibit apoptosis. Therefore, we studied the expression of SATB1 in SCLC. Methods: The level of SATB1 was analyzed in SCLC tissues, metastatic lymphoid nodes and adjacent normal lung tissues by immunohistochemistry. Meanwhile, small interfering SATB1-targeting RNA was constructed and transfected into human SCLC cell line NCI-H446 to evaluate the effects of SATB1-siRNA on cell proliferation, invasion and apoptosis. Result: SATB1 protein was overexpressed in SCLC tissues and metastasis lymphoid nodes compared with adjacent normal lung tissues. Compared with control group, SATB1-siRNA inhibits the proliferation and invasion of SCLC cells and induces SCLC cells apoptosis statistically (P<0.05) in vitro. Conclusion: Our results suggest that SATB1 plays an important role in the metastasis of human SCLC cell.
-
Silencing SATB1 with siRNA inhibits the proliferation and invasion of small cell lung cancer cells
Cancer cell international, 2013Co-Authors: Bo Huang, Xiaodong Wang, Hongli Zhou, Zhiliang LiuAbstract:Background: Small cell lung cancer (SCLC) is a special kind of lung cancers, lymph or blood metastasis of SCLC usually occurs in early stage. Studies in breast and colon cancer showed over expression of SATB1 could promote tumor cell growth and inhibit apoptosis. Therefore, we studied the expression of SATB1 in SCLC. Methods: The level of SATB1 was analyzed in SCLC tissues, metastatic lymphoid nodes and adjacent normal lung tissues by immunohistochemistry. Meanwhile, small interfering SATB1-targeting RNA was constructed and transfected into human SCLC cell line NCI-H446 to evaluate the effects of SATB1-siRNA on cell proliferation, invasion and apoptosis. Result: SATB1 protein was overexpressed in SCLC tissues and metastasis lymphoid nodes compared with adjacent normal lung tissues. Compared with control group, SATB1-siRNA inhibits the proliferation and invasion of SCLC cells and induces SCLC cells apoptosis statistically (P
Takeshi Senga - One of the best experts on this subject based on the ideXlab platform.
-
SATB1 and satb2 play opposing roles in c myc expression and progression of colorectal cancer
Oncotarget, 2016Co-Authors: Mohammed A Mansour, Toshinori Hyodo, Khondker Ayesha Akter, Keisuke Uehara, Toshio Kokuryo, Masato Nagino, Takeshi SengaAbstract:// Mohammed A. Mansour 1, 2 , Toshinori Hyodo 1 , Khondker Ayesha Akter 1 , Toshio Kokuryo 3 , Keisuke Uehara 3 , Masato Nagino 3 , Takeshi Senga 1 1 Division of Cancer Biology, Nagoya University Graduate School of Medicine, Showa, Nagoya, 466-8550 Japan 2 Biochemistry Section, Department of Chemistry, Faculty of Science, Tanta University, Tanta 31527, Egypt 3 Department of Surgical Oncology, Nagoya University Graduate School of Medicine, Showa, Nagoya, 466-8550 Japan Correspondence to: Mohammed A. Mansour, e-mail: biomansour@hotmail.com Keywords: colorectal cancer, SATB2, c-Myc, SATB1 Received: August 13, 2015 Accepted: December 05, 2015 Published: December 18, 2015 ABSTRACT Special AT-rich sequence-binding protein 1 and 2 (SATB1/2) are nuclear matrix-associated proteins involved in chromatin remodeling and regulation of gene expression. SATB2 acts as a tumor suppressor in laryngeal squamous cell carcinoma and colon cancer, whereas SATB1 promotes the progression of numerous types of cancers. In this study, we examined the effects of SATB1 and SATB2 on the malignant characteristics of colorectal cancer cells. SATB1 and SATB2 expression were negatively correlated in colorectal cancer specimens. SATB1 expression was increased, whereas SATB2 expression was reduced, in colorectal cancer tissues compared to control tissues. Exogenous expression of SATB2 in colorectal cancer cells suppressed cell proliferation, colony formation and tumor proliferation in mice. c-Myc was reduced by SATB2 expression, and exogenous expression of c-Myc in SATB2-expressing cells restored proliferation, colony formation and in vivo tumor growth of colorectal cancer cells. We also showed that c-Myc reduction by SATB2 was mediated by the inactivation of ERK5. In contrast, SATB1 promoted c-Myc expression. The expression of SATB1 in colorectal cancer tissues was positively correlated with c-Myc expression, and SATB1 knockdown reduced c-Myc expression in colorectal cancer cells. Finally, we showed that SATB1 knockdown in colorectal cancer cells suppressed cell proliferation, colony formation and cell invasion. Our results reveal interesting features of how the structural homologs SATB1 and SATB2 exert opposing functions in colorectal tumorigenesis.
-
SATB1 and SATB2 play opposing roles in c-Myc expression and progression of colorectal cancer
Oncotarget, 2015Co-Authors: Mohammed A Mansour, Toshinori Hyodo, Khondker Ayesha Akter, Keisuke Uehara, Toshio Kokuryo, Masato Nagino, Takeshi SengaAbstract:Special AT-rich sequence-binding protein 1 and 2 (SATB1/2) are nuclear matrix-associated proteins involved in chromatin remodeling and regulation of gene expression. SATB2 acts as a tumor suppressor in laryngeal squamous cell carcinoma and colon cancer, whereas SATB1 promotes the progression of numerous types of cancers. In this study, we examined the effects of SATB1 and SATB2 on the malignant characteristics of colorectal cancer cells. SATB1 and SATB2 expression were negatively correlated in colorectal cancer specimens. SATB1 expression was increased, whereas SATB2 expression was reduced, in colorectal cancer tissues compared to control tissues. Exogenous expression of SATB2 in colorectal cancer cells suppressed cell proliferation, colony formation and tumor proliferation in mice. c-Myc was reduced by SATB2 expression, and exogenous expression of c-Myc in SATB2-expressing cells restored proliferation, colony formation and in vivo tumor growth of colorectal cancer cells. We also showed that c-Myc reduction by SATB2 was mediated by the inactivation of ERK5. In contrast, SATB1 promoted c-Myc expression. The expression of SATB1 in colorectal cancer tissues was positively correlated with c-Myc expression, and SATB1 knockdown reduced c-Myc expression in colorectal cancer cells. Finally, we showed that SATB1 knockdown in colorectal cancer cells suppressed cell proliferation, colony formation and cell invasion. Our results reveal interesting features of how the structural homologs SATB1 and SATB2 exert opposing functions in colorectal tumorigenesis.
Bo Huang - One of the best experts on this subject based on the ideXlab platform.
-
Effect of SATB1 silencing on the proliferation, invasion and apoptosis of TE-1 esophageal cancer cells
Oncology letters, 2017Co-Authors: Bo Huang, Fei Xiong, Siwang Wang, Xianping Lang, Xiaodong Wang, Hongli ZhouAbstract: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.
-
silencing SATB1 with sirna inhibits the proliferation and invasion of small cell lung cancer cells
Cancer Cell International, 2013Co-Authors: Bo Huang, Xiaodong Wang, Hongli Zhou, Zhiliang LiuAbstract:Background: Small cell lung cancer (SCLC) is a special kind of lung cancers, lymph or blood metastasis of SCLC usually occurs in early stage. Studies in breast and colon cancer showed over expression of SATB1 could promote tumor cell growth and inhibit apoptosis. Therefore, we studied the expression of SATB1 in SCLC. Methods: The level of SATB1 was analyzed in SCLC tissues, metastatic lymphoid nodes and adjacent normal lung tissues by immunohistochemistry. Meanwhile, small interfering SATB1-targeting RNA was constructed and transfected into human SCLC cell line NCI-H446 to evaluate the effects of SATB1-siRNA on cell proliferation, invasion and apoptosis. Result: SATB1 protein was overexpressed in SCLC tissues and metastasis lymphoid nodes compared with adjacent normal lung tissues. Compared with control group, SATB1-siRNA inhibits the proliferation and invasion of SCLC cells and induces SCLC cells apoptosis statistically (P<0.05) in vitro. Conclusion: Our results suggest that SATB1 plays an important role in the metastasis of human SCLC cell.
-
Silencing SATB1 with siRNA inhibits the proliferation and invasion of small cell lung cancer cells
Cancer cell international, 2013Co-Authors: Bo Huang, Xiaodong Wang, Hongli Zhou, Zhiliang LiuAbstract:Background: Small cell lung cancer (SCLC) is a special kind of lung cancers, lymph or blood metastasis of SCLC usually occurs in early stage. Studies in breast and colon cancer showed over expression of SATB1 could promote tumor cell growth and inhibit apoptosis. Therefore, we studied the expression of SATB1 in SCLC. Methods: The level of SATB1 was analyzed in SCLC tissues, metastatic lymphoid nodes and adjacent normal lung tissues by immunohistochemistry. Meanwhile, small interfering SATB1-targeting RNA was constructed and transfected into human SCLC cell line NCI-H446 to evaluate the effects of SATB1-siRNA on cell proliferation, invasion and apoptosis. Result: SATB1 protein was overexpressed in SCLC tissues and metastasis lymphoid nodes compared with adjacent normal lung tissues. Compared with control group, SATB1-siRNA inhibits the proliferation and invasion of SCLC cells and induces SCLC cells apoptosis statistically (P
Rafeeq Mir - One of the best experts on this subject based on the ideXlab platform.
-
wnt β catenin signaling regulated SATB1 promotes colorectal cancer tumorigenesis and progression
Oncogene, 2016Co-Authors: Rafeeq Mir, Saurabh J. Pradhan, Prithviraj Patil, R. Mulherkar, Sanjeev GalandeAbstract: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.
-
Wnt/β-catenin signaling regulated SATB1 promotes colorectal cancer tumorigenesis and progression.
Oncogene, 2015Co-Authors: Rafeeq Mir, Saurabh J. Pradhan, Prithviraj Patil, R. Mulherkar, Sanjeev GalandeAbstract: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.
-
Wnt/β-catenin signaling regulated SATB1 promotes colorectal cancer
2015Co-Authors: Rafeeq Mir, Saurabh J. Pradhan, Prithviraj Patil, R. Mulherkar, Sanjeev GalandeAbstract: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.