Characterisation of chicken TES and its role in cell spreading and motility

Griffith, Elen; Coutts, Amanda S.; Black, Donald M.

doi:10.1002/cm.10162

Cited by 27 publications

(36 citation statements)

References 30 publications

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“…When human TES was overexpressed in Rat-1 fibroblasts, and when chicken TES (cTES) was overexpressed in chicken embryo fibroblasts (CEF), cells showed increased spreading on fibronectin [Coutts et al, 2003;Griffith et al, 2004]. Additionally, expression of human TES in T47D cells and overexpression of cTES in CEF, resulted in decreased cell motility [Griffith et al, 2004] (Coutts et al, unpublished data). These data suggest that TES plays a role in events related to regulation of the cytoskeleton leading to changes in cell spreading and motility.…”

Section: Introductionmentioning

confidence: 93%

“…LIM domains are believed to mediate protein-protein interactions and to act as molecular scaffolds [Arber and Caroni, 1996]. Indeed, TES has been shown to have a range of interacting partners including the cytoskeletal proteins zyxin, talin, mena, VASP, and actin [Coutts et al, 2003;Garvalov et al, 2003;Griffith et al, 2004].…”

Section: Introductionmentioning

confidence: 99%

“…We, and others, have shown that TES is a novel focal adhesion protein localising to cell-cell adhesions, actin stress fibres, as well as cell-matrix adhesions [Coutts et al, 2003;Garvalov et al, 2003;Griffith et al, 2004]. TES contains three carboxyl (C)-terminal LIM domains that are double zinc finger motifs with the consensus sequence CX 2 CX 17-19 HX 2 (C/H)X 2 CX 2 CX 17-19 CX 2 (C/H/D) [Dawid et al, 1998].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

RNAi knockdown of the focal adhesion protein TES reveals its role in actin stress fibre organisation

Griffith

Coutts

Black

2005

Cell Motil. Cytoskeleton

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TES was originally identified as a candidate tumour suppressor gene and has subsequently been found to encode a novel focal adhesion protein. As well as localising to cell-matrix adhesions, TES localises to cell-cell contacts and to actin stress fibres. TES interacts with a variety of cytoskeletal proteins including zyxin, mena, VASP, talin and actin. There is evidence that TES may function in actin-dependent processes as overexpression of TES results in increased cell spreading and decreased cell motility. Together with TES's interacting partners, these data suggest that TES might be involved in regulation of the actin cytoskeleton. Here, for the first time, we have used RNAi to successfully knockdown TES in HeLa cells and we demonstrate that loss of TES from focal adhesions results in loss of actin stress fibres. Similarly, and as previously reported, RNAi-mediated knockdown of zyxin results in loss of actin stress fibres. TES siRNA treated cells show reduced RhoA activity, suggesting that the Rho GTPase pathway may be involved in the TES RNAi-induced loss of stress fibres. We have also used RNAi to examine the requirement of TES and zyxin for each other's localisation at focal adhesions, and we propose a hierarchy of recruitment, with zyxin being first, followed by VASP and then TES. Cell Motil.

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Section: Introductionmentioning

confidence: 93%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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RNAi knockdown of the focal adhesion protein TES reveals its role in actin stress fibre organisation

Griffith

Coutts

Black

2005

Cell Motil. Cytoskeleton

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“…In mice, TES interacts and colocalises with a variety of cytoskeletal proteins, including zyxin, mena, VASP, talin and actin (36,37). Overexpression of TES decreased cell motility (36)(37)(38). Moreover, restoration of TES expression in breast cancer and uterine sarcoma cell lines inhibited their growth by induction of apoptosis (34).…”

Section: Introductionmentioning

confidence: 99%

Differential expression of testin and survivin in breast cancer subtypes

et al. 2013

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Abstract. Testin (TES) is a putative tumour-suppressor gene downregulated in various types of cancers. Survivin is a nodal protein involved in multiple signalling pathways, tumour maintenance and inhibition of apoptosis. Previous studies indicate that TES and survivin can functionally interact and modulate cell death and proliferation in breast cancer cells. The aim of the present study was to investigate the expression and prognostic relevance of TES and survivin in breast cancer subtypes examining a large cohort of breast cancer patients. We determined the expression of TES and survivin by immunohistochemistry (IHC) in tissue samples from 242 breast cancer patients diagnosed between 1981 and 2009. The expression of these proteins was compared with clinical and pathological data. There was a significant association of nuclear survivin overexpression and TES downregulation with triple-negative tumours [P=0.009; univariate odds ratio (OR), 3.20; 95% CI, 1.34-7.66] (P=0.018; multivariate OR, 2.90; 95% CI, 1.20-6.97). A further significant correlation was observed between TES downregulation and the luminal B subtype (P=0.019, univariate OR: 2.90; 95% CI, 1.19-7.06) (P=0.032, multivariate OR, 2.67; 95% CI, 1.09-6.65), independent of survivin expression. Our results demonstrated a statistically significant association between TES downregulation and highly aggressive breast tumour subtypes, such as triplenegative and luminal B tumours, along with the prognostic relevance of nuclear expression of survivin. To our knowledge, this is the first demonstration of such an association.

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“…Tes overexpression enhanced cell spreading and decreased cell motility (10). RNA interference knockdown of Tes led to a loss of actin stress fibers, suggesting a role of the protein in actin cytoskeleton regulation (11).…”

mentioning

confidence: 96%

Knockout mice reveal a tumor suppressor function for Testin

Drusco

Zanesi

Roldo

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

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The Testin (TES) gene was previously identified as a putative human tumor suppressor gene at 7q31.2, a region that is frequently deleted in hematopoietic malignancies, as well as in epithelial tumors. To determine whether TES acts as a tumor suppressor in vivo, we generated a Tes knockout mouse and then used it in an established model of carcinogen-induced gastric cancer. In mice a zinc-deficient (ZD) diet enhances cellular proliferation in the forestomach and susceptibility to N-nitrosomethylbenzylamine (NMBA)-induced carcinogenesis. Five-week-old Tes wild-type (؉͞؉), heterozygous (؉͞؊), and homozygous (؊͞؊) mice were divided into four groups: mice fed a zinc-sufficient diet (ZS); mice fed a ZD diet; ZS fed plus NMBA-treated mice (ZS؉NMBA), and ZD fed plus NMBA-treated mice (ZD؉NMBA). After 4 weeks, the ZS؉NMBA and ZD؉NMBA groups were treated with three intragastric doses of NMBA. Animals were killed 8 weeks after NMBA administration: 25% of ؉͞؉ mice developed benign lesions; 88% of ؉͞؊ showed multiple papillomas, atypical glandular metaplasia, and squamous cell carcinomasl; and 81% of ؊͞؊ mice displayed very large papillomas, squamous cell carcinomas, and adenocarcinomas. A statistically significant difference in tumor incidence was found between ؉͞؊ versus ؉͞؉ and ؊͞؊ versus ؉͞؉ (P < 0.0001). These data suggest that Tes functions as a tumor suppressor gene in vivo.carcinogen-induced tumorigenesis ͉ gastric cancer ͉ TES ͉ gene targeting

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Characterisation of chicken TES and its role in cell spreading and motility

Cited by 27 publications

References 30 publications

RNAi knockdown of the focal adhesion protein TES reveals its role in actin stress fibre organisation

RNAi knockdown of the focal adhesion protein TES reveals its role in actin stress fibre organisation

Differential expression of testin and survivin in breast cancer subtypes

Knockout mice reveal a tumor suppressor function for Testin

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