S100A6 is transcriptionally regulated by β-catenin and interacts with a novel target, lamin A/C, in colorectal cancer cells

Kilańczyk, Ewa; Graczyk, Agnieszka; Ostrowska, H; Kasacka, Irena; Leśniak, Wiesława; Filipek, Anna

doi:10.1016/j.ceca.2012.04.005

Cited by 33 publications

(25 citation statements)

References 34 publications

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“…S100A6 protein was also established as a novel interacting partner of lamin A/C protein, hence potentially linking lamin A/C in colorectal cancer development and progression. 23 This clearly indicates that improper regulation of lamins leads to various type of gastrointestinal cancers, in later section of the review we shall discuss other form of gastrointestinal cancers also.…”

Section: Role Of Lamins In Colorectal Cancermentioning

confidence: 99%

A novel role of lamins from genetic disease to cancer biomarkers

Sakthivel¹,

Sehgal²

2016

Oncol Rev

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Lamins are the key components of the nuclear lamina and by virtue of their interactions with chromatin and binding partners act as regulators of cell proliferation and differentiation. Of late, the diverse roles of lamins in cellular processes have made them the topic of intense debate for their role in cancer progression. The observations about aberrant localization or misexpression of the nuclear lamins in cancerous tissues have often led to the speculative role of lamins as a cancer risk biomarker. Here we discuss the involvement of lamins in several cancer subtypes and their potential role in predicting the tumor progression.

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Section: Role Of Lamins In Colorectal Cancermentioning

confidence: 99%

A novel role of lamins from genetic disease to cancer biomarkers

Sakthivel¹,

Sehgal²

2016

Oncol Rev

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“…S100A6 is upregulated and correlated with Dukes' tumor stage or lymphatic permeation in CRC (15,16). S100A6 is transcriptionally regulated by β-catenin, a key effector of Wnt/β-catenin signaling pathway that is abnormally activated in CRC (17). However, the effect of S100A6 on CRC and the underlying molecular mechanisms are still elusive.…”

Section: Introductionmentioning

confidence: 99%

S100A6 stimulates proliferation and migration of colorectal carcinoma cells through activation of the MAPK pathways

Duan

Zou

et al. 2013

International Journal of Oncology

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The S100A6 protein, a member of the S100 protein family, is overexpressed in many tumors including colorectal carcinoma (CRC). Although recent studies showed that the elevated expression of S100A6 was associated with the stage and lymphatic permeation of CRC, little is known about whether and how S100A6 contributes to CRC development. Here we investigated the S100A6 expression in CRC tissues and cell lines, and explored the molecular mechanisms underlying the role of S100A6 in CRC development by examining cell proliferation and migration in vitro, and tumorigenicity in nude mice. The results show that S100A6 expression was markedly increased in CRC tissues and cell lines compared to normal colon tissues and a normal colon mucosal epithelial cell line, respectively. Recombinant adenovirus-mediated overexpression of S100A6 or treatment with recombinant S100A6 protein in HCT116, a CRC cell line with relative low S100A6 expression, resulted in enhanced cell proliferation and migration, and the mitogen-activated protein kinase (MAPK) activation in vitro, and tumor growth in vivo. Conversely, RNAi-mediated knockdown of S100A6 in LoVo, a CRC cell line with relative high S100A6 expression, resulted in reduced cell proliferation, migration and MAPK activity. S100A6-induced proliferation was partially attenuated by an ERK inhibitor while migration was suppressed by a p38 inhibitor. Taken together, our results suggest that the cellular effects of S100A6 are mediated by the ERK and p38 MAPK pathways, and modulation of these pathways may be employed for CRC prevention and therapy.

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“…Kilanczyk et al (31) observed that the expression of S100A6 was regulated by β-catenin in colorectal cancer cells, suggesting that the S100A6 gene may be a transcriptional target of β-catenin. In addition, reduced β-catenin levels have been reported in HepG2.2.15 cells, which result in decreased S100A6 levels (32).…”

Section: Discussionmentioning

confidence: 99%

Effects of S100A6 gene silencing on the biological features of eutopic endometrial stromal cells and β-catenin expression

Xiao-ling

Liu

Chen

et al. 2017

Molecular Medicine Reports

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Protein expression levels of S100 calcium binding protein A6 (S100A6) are increased in various malignancies and are associated with tumor behavior; however, the association between S100A6 and endometriosis remains to be elucidated. In order to investigate the influence of S100A6 protein, recombinant lentivirus siS100A6 was used to transfect the eutopic endometrial stromal cells. CCK-8 assay was performed to identify the proliferation ability of cell and the cell migration was detected by Transwell assay. Flow cytometry was performed to detect cell apoptosis, and western blotting and reverse transcription-quantitative polymerase chain reaction were performed to identify the expression of β-catenin. The present study investigated the role of S100A6 in endometriosis and its interaction with β-catenin by transfecting eutopic endometrial stromal cells with a recombinant lentivirus containing S100A6-specific small interfering RNA. Inhibition of S100A6 expression had a significant antiproliferative effect and reduced the migratory ability of eutopic endometrial stromal cells, and induced their apoptosis. In addition, inhibition of S100A6 expression suppressed β-catenin expression. These results suggested that inhibition of S100A6 may represent a promising novel approach for the targeted therapy of endometriosis.

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S100A6 is transcriptionally regulated by β-catenin and interacts with a novel target, lamin A/C, in colorectal cancer cells

Cited by 33 publications

References 34 publications

A novel role of lamins from genetic disease to cancer biomarkers

A novel role of lamins from genetic disease to cancer biomarkers

S100A6 stimulates proliferation and migration of colorectal carcinoma cells through activation of the MAPK pathways

Effects of S100A6 gene silencing on the biological features of eutopic endometrial stromal cells and β-catenin expression

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