Association of the mammalian transcriptional regulator Kaiso with centrosomes and the midbody

Kantidze, Omar L.; Kamalyukova, Ilnaz M.; Razin, Sergey V.

doi:10.4161/cc.8.14.8944

Cited by 13 publications

(18 citation statements)

References 17 publications

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“…Recent studies in cancer have examined localization of Kaiso in relation to p120. Overall, they indicated that nuclear Kaiso localization is decreased when p120 resides in the cytosol, although it appeared that the expression of Kaiso and its localization are highly variable, and depend on the cellular context and type of tumor examined (Soubry et al, 2005;Kantidze et al, 2009;Soubry et al, 2010;Zhang et al, 2011;Vermeulen et al, 2012). Notwithstanding this high variability, several bona fide Kaiso targets (e.g.…”

Section: The Role Of Kaiso In Cancermentioning

confidence: 90%

p120-catenin in cancer – mechanisms, models and opportunities for intervention

Schackmann

Tenhagen

Ven

et al. 2013

Journal of Cell Science

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The epithelial adherens junction is an E-cadherin-based complex that controls tissue integrity and is stabilized at the plasma membrane by p120-catenin (p120, also known as CTNND1). Mutational and epigenetic inactivation of E-cadherin has been strongly implicated in the development and progression of cancer. In this setting, p120 translocates to the cytosol where it exerts oncogenic properties through aberrant regulation of Rho GTPases, growth factor receptor signaling and derepression of Kaiso (also known as ZBTB33) target genes. In contrast, indirect inactivation of the adherens junction through conditional knockout of p120 in mice was recently linked to tumor formation, indicating that p120 can also function as a tumor suppressor. Supporting these opposing functions are findings in human cancer, which show that either loss or cytoplasmic localization of p120 is a common feature in the progression of several types of carcinoma. Underlying this dual biological phenomenon might be the context-dependent regulation of Rho GTPases in the cytosol and the derepression of Kaiso target genes. Here, we discuss past and present findings that implicate p120 in the regulation of cancer progression and highlight opportunities for clinical intervention.

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Section: The Role Of Kaiso In Cancermentioning

confidence: 90%

p120-catenin in cancer – mechanisms, models and opportunities for intervention

Schackmann

Tenhagen

Ven

et al. 2013

Journal of Cell Science

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“…In contrast to β-catenin, the role of CTNND1 has been less elucidated. CTNND1 first attracted attention when the known transcriptional factor Kaiso was identified as a CTNND1-specific binding partner [ 11 ]. Kaiso inhibits β-catenin/TCF activation of target genes, and CTNND1 inhibits Kaiso activity.…”

Section: Introductionmentioning

confidence: 99%

“…Kaiso inhibits β-catenin/TCF activation of target genes, and CTNND1 inhibits Kaiso activity. Thus, it is now thought that the Kaiso/CTNND1 complex is a modulator of the canonical Wnt/β-catenin signaling pathway [ 11 ]. Recently, a large amount of data has implicated CTNND1 in the regulation of cancer development and progression [ 12 – 14 ].…”

Section: Introductionmentioning

confidence: 99%

Overexpression of CTNND1 in hepatocellular carcinoma promotes carcinous characters through activation of Wnt/β-catenin signaling

Tang

Wang

et al. 2016

J Exp Clin Cancer Res

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BackgroundIncreasing evidence supports the association of CTNND1 with tumor development and progression. However, the mechanism and clinical significance of CTNND1 deregulation in hepatocellular carcinoma (HCC) remains unknown. In this study, we aim to investigate the role of CTNND1 in HCC.MethodsqRT-PCR and immunohistochemical analyses were used to measure the levels of CTNND1 in HCC specimens and HCC cell lines. CTNND1 and shCTNND1 were transfected into HCC cell lines to investigate its role in HCC. Cell migration and invasion were measured by Transwell and Matrigel analyses in vitro. In vivo metastasis assays were performed in SCID mice.ResultsIn clinical HCC samples, we found that CTNND1 expression was significantly up-regulated in cancer lesions compared with paired normal liver tissues. By silencing or overexpressing CTNND1 in HCC cells, we found that CTNND1 could promote cell proliferation, migration, and invasion in vitro. An in-vivo assay showed that CTNND1 dramatically promoted HCC cell tumor formation and metastasis. Moreover, CTNND1 promoted HCC metastasis, at least in part, by indirectly enhancing Wnt/β-catenin signaling. Consistent with these results, the expression of CTNND1 was positively correlated with β-catenin, WNT11, Cyclin D1, and BMP7 expression in human HCC specimens.ConclusionsOur study provides evidence that CTNND1 functions as a novel tumor oncogene in HCC, and may be a potential therapeutic target for HCC management.Electronic supplementary materialThe online version of this article (doi:10.1186/s13046-016-0344-9) contains supplementary material, which is available to authorized users.

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“…106,107 At centrosomes, p120-catenin colocalizes and associates with cyclin E and cyclin-dependent kinase 2, key proteins involved in centrosome duplication during mitosis. 108 Interestingly, the transcription factor Kaiso, originally described as a binding partner of p120-catenin, 109 also localizes to centrosomes, mitotic spindles and the midbody, 110,111 and colocalizes with p120-catenin at spindle poles in HeLa cells. 110 Through these novel connections, and the roles of p120-catenin in the regulation of RhoGTPases and the cytoskeleton, 112,113 p120-catenin may potentially regulate centrosomal and mitotic spindle functions and integrity.…”

Section: Links Between Cadherin-catenins and Positioning Of Mitotic Smentioning

confidence: 99%

“…108 Interestingly, the transcription factor Kaiso, originally described as a binding partner of p120-catenin, 109 also localizes to centrosomes, mitotic spindles and the midbody, 110,111 and colocalizes with p120-catenin at spindle poles in HeLa cells. 110 Through these novel connections, and the roles of p120-catenin in the regulation of RhoGTPases and the cytoskeleton, 112,113 p120-catenin may potentially regulate centrosomal and mitotic spindle functions and integrity. Indeed decreased levels of p120-catenin in epidermal cells lead to alterations in centrosomes and spindles, mitotic defects and aneuplody in a cell autonomous manner.…”

Section: Links Between Cadherin-catenins and Positioning Of Mitotic Smentioning

confidence: 99%

Connections between cadherin-catenin proteins, spindle misorientation, and cancer

Shahbazi

Pérez-Moreno

2015

Tissue Barriers

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Association of the mammalian transcriptional regulator Kaiso with centrosomes and the midbody

Cited by 13 publications

References 17 publications

p120-catenin in cancer – mechanisms, models and opportunities for intervention

p120-catenin in cancer – mechanisms, models and opportunities for intervention

Overexpression of CTNND1 in hepatocellular carcinoma promotes carcinous characters through activation of Wnt/β-catenin signaling

Connections between cadherin-catenin proteins, spindle misorientation, and cancer

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