Reduced expression and aberrant localization of p120catenin in human squamous cell carcinoma of the skin

Ishizaki, Yasuko; Omori, Yasufumi; Momiyama, Megumi; Nishikawa, Yuji; Tokairin, Takuo; Manabe, Motomu; Enomoto, Katsuhiko

doi:10.1016/j.jdermsci.2003.12.001

Cited by 27 publications

(24 citation statements)

References 25 publications

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“…The present study showed that reduced or absent expression of E-cadherin and P120 was associated with the histological grade of tumors, which is consistent with reported data [17][18][19][20][21] . In well-differentiated tumors, there were obvious and strong staining along the cell-cell boundaries, whereas in poorly-differentiated tumors, the immunohistostaining was focally and heterogeneously distributed, with patchy or spotty features along the cellcell boundaries, indicating that the staining of E-cadheri and P120 is related with the differentiation of ICC, namely both E-cadherin and P120 may be regarded as differentiation markers of tumor.…”

Section: Discussionsupporting

confidence: 93%

Reduced expression of P120 catenin in cholangiocarcinoma correlated with tumor clinicopathologic parameters

Zhai¹,

Yan²,

Li³

et al. 2008

WJG

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AIM: To i nve s t i g a t e t h e re l a t i o n s h i p b e t w e e n the expression of P120 and the clinicopathologic parameters in intrahepatic cholangiocarcinoma (ICC). METHODS: An immunohistochemical study of E-cadherin and P120 catenin was performed on 42 specimens of ICC with a Dako Envision kit. RESULTS: The expression of E-cadherin and P120 was reduced in 27 cases (64.3%) and 31 cases (73.8%), respectively. Both E-cadherin and P120 expressions were significantly correlated with the tumor histological grade (χ 2 = 9.333, P = 009 and χ 2 = 11.71, P = 0.003), TNM stage (χ 2 = 8.627, P = 0.035 and χ 2 = 13.123, P = 0.004), intrahepatic metastasis (χ 2 = 7.292, P = 0.007 and χ 2 = 4.657, P = 0.041, respectively) and patients' survival (χ 2 = 6.351, P = 0.002 and χ 2 = 4.023, P = 0.000, respectively). In addition, the expression of P120 was in concordance with that of E-cadherin ( χ 2 = 1 3 .7 9 7, P = 0 . 0 0 0 ) , i n d i c a t i n g t h a t t h e expression of P120 may be dependent on that of E-cadherin. Finally, only P120 expression was found to be an independent prognostic factor in Cox regression model (r = 0.088, P = 0.049). CONCLUSION:D o w n-re g u la t e d e x p re s s io n o f E-cadherin and P120 occurs frequently in ICC and contributes to the progression and development of tumor. Both of them may be valuable biologic markers for predicting tumor invasion, metastasis and patients' survival, but only P120 is an independent prognostic factor for ICC.

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Section: Discussionsupporting

confidence: 93%

Reduced expression of P120 catenin in cholangiocarcinoma correlated with tumor clinicopathologic parameters

Zhai¹,

Yan²,

Li³

et al. 2008

WJG

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“…As has been extensively reported for E-cadherin, p120-catenin expression is also frequently reduced to very low or undetectable levels in the major human carcinoma types (45), including the squamous cell carcinoma with poor differentiation (46). In the normal human epidermis, p120-catenin is expressed faintly in the stratum basale but intensely in the stratum granulosum and finally disappears in the stratum corneum (46), which correlates with the epidermal differentiation. In our present study we sought to examine the potential contribution of E-cadherin/catenin-activated PI3K to the PLC-␥1 activation by calcium and determine whether this signaling pathway is required for calcium-induced human keratinocyte differentiation.…”

mentioning

confidence: 62%

“…Unlike ␤-and ␥-catenin, p120-catenin does not interact with ␣-catenin (44). As has been extensively reported for E-cadherin, p120-catenin expression is also frequently reduced to very low or undetectable levels in the major human carcinoma types (45), including the squamous cell carcinoma with poor differentiation (46). In the normal human epidermis, p120-catenin is expressed faintly in the stratum basale but intensely in the stratum granulosum and finally disappears in the stratum corneum (46), which correlates with the epidermal differentiation.…”

mentioning

confidence: 87%

The Recruitment of Phosphatidylinositol 3-Kinase to the E-cadherin-Catenin Complex at the Plasma Membrane Is Required for Calcium-induced Phospholipase C-γ1 Activation and Human Keratinocyte Differentiation

Xie

Bikle

2007

Journal of Biological Chemistry

102

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Calcium induces epidermal keratinocyte differentiation, but the mechanism is not completely understood. We have previously demonstrated that calcium-induced human keratinocyte differentiation requires an intracellular calcium rise caused by phosphatidylinositol 3-kinase (PI3K)-dependent activation of phospholipase C-␥1. In this study we sought to identify the upstream signaling pathway necessary for calcium activation of PI3K and its subsequent activation of phospholipase C-␥1. We found that calcium induces the recruitment of PI3K to the E-cadherin-catenin complex at the plasma membrane of human keratinocytes. Knocking-down E-cadherin, ␤-catenin, or p120-catenin expression blocked calcium activation of PI3K and phospholipase C-␥1 and calcium-induced keratinocyte differentiation. However, knocking-down ␥-catenin expression had no effect. Calcium-induced PI3K recruitment to E-cadherin stabilized by p120-catenin at the plasma membrane requires ␤-catenin but not ␥-catenin. These data indicate that the recruitment of PI3K to the E-cadherin/␤-catenin/p120-catenin complex via ␤-catenin at the plasma membrane is required for calcium-induced phospholipase C-␥1 activation and, ultimately, keratinocyte differentiation.

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“…A431 cells in common with most epithelial cells, predominantly express p120 isoform 3 (Ishizaki et al, 2004). Therefore constructs encoding murine p120 isoform 3A were reintroduced into cells in which p120 had been knocked down.…”

Section: Rnai-mediated Knockdown and Reconstitution Of P120mentioning

confidence: 99%

p120-catenin is required for the collective invasion of squamous cell carcinoma cells via a phosphorylation-independent mechanism

et al. 2007

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Loss of E-cadherin-mediated cell-cell junctions has been correlated with cancer cell invasion and poor patient survival. p120-catenin has emerged as a key player in promoting E-cadherin stability and adherens junction integrity and has been proposed as a potential invasion suppressor by preventing release of cells from the constraints imposed by cadherin-mediated cell-cell adhesion. However, it has been proposed that tyrosine phosphorylation of p120 may contribute to cadherindependent junction disassembly during invasion. Here, we use small interfering RNA (siRNA) in A431 cells to show that knockdown of p120 promotes two-dimensional migration of cells. In contrast, p120 knockdown impairs epidermal growth factor-induced A431 invasion into threedimensional matrix gels or in organotypic culture, whereas re-expression of siRNA-resistant p120, or a p120 isoform that cannot be phosphorylated on tyrosine, restores the collective mode of invasion employed by A431 cells in vitro. Thus, p120 promotes A431 cell invasion in a phosphorylation-independent manner. We show that the collective invasion of A431 cells depends on the presence of cadherin-mediated (P-and E-cadherin) cell-cell contacts, which are lost in cells where p120 expression is knocked down. Furthermore, membranous p120 is maintained in invasive squamous cell carcinomas in tumours suggesting that p120 may be important for the collective invasion of tumours cells in vivo.

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Reduced expression and aberrant localization of p120catenin in human squamous cell carcinoma of the skin

Cited by 27 publications

References 25 publications

Reduced expression of P120 catenin in cholangiocarcinoma correlated with tumor clinicopathologic parameters

Reduced expression of P120 catenin in cholangiocarcinoma correlated with tumor clinicopathologic parameters

The Recruitment of Phosphatidylinositol 3-Kinase to the E-cadherin-Catenin Complex at the Plasma Membrane Is Required for Calcium-induced Phospholipase C-γ1 Activation and Human Keratinocyte Differentiation

p120-catenin is required for the collective invasion of squamous cell carcinoma cells via a phosphorylation-independent mechanism

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