α-catenin

Sun, Yutong; Zhang, Jinsong; Ma, Li

doi:10.4161/cc.29765

Cited by 33 publications

(23 citation statements)

References 60 publications

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“…CNLs in A1 105-124 Mb, and D2 54-88.9 Mb) also detected in normal-like TN-FMCs. Among genes deleted, tumour suppressor CTNNA1 (A1 105-124 Mb, human homologue in HSA 5q) is implicated in cell-cell adhesion maintainance and regulation of multiple signalling pathways in human cancer 106 . Furthermore, CNLs affecting the basal-like TN-FMCs enriched the basal cell carcinoma pathway, and the Wnt signalling pathway commonly deregulated in hTNBCs 28,77,106 .…”

Section: Discussionmentioning

confidence: 99%

Analysis of Copy-Number Variations and Feline Mammary Carcinoma Survival

Granados-Soler

Bornemann-Kolatzki²,

Beck³

et al. 2020

Sci Rep

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Feline mammary carcinomas (FMCs) are highly malignant. As the disease-free survival (DFS) and overall survival (OS) are short, prognostication is crucial. Copy-number variations (CNVs) analysis by nextgeneration sequencing serves to identify critical cancer-related genomic regions. Thirty-three female cats with FMCs were followed during two years after surgery. Tumours represented tubulopapillary and solid carcinomas encompassing six molecular subtypes. Regardless of the histopathological diagnosis, molecular subtypes showed important differences in survival. Luminal A tumours exhibited the highest DFS (p = 0.002) and cancer-specific OS (p = 0.001), and the lowest amount of CNVs (p = 0.0001). In contrast, basal-like triple-negative FMCs had the worst outcome (DFS, p < 0.0001; and OS, p < 0.00001) and were the most aberrant (p = 0.05). In the multivariate analysis, copy-number losses (CNLs) in chromosome B1 (1-23 Mb) harbouring several tumour-repressors (e.g. CSMD1, MTUS1, MSR1, DBC2, and TUSC3) negatively influenced DFS. Whereas, copy-number gains (CNGs) in B4 (1-29 Mb) and F2 (64-82.3 Mb) comprising epithelial to mesenchymal transition genes and metastasis-promoting transcription factors (e.g. GATA3, VIM, ZEB1, and MYC) negatively influenced DFS and cancer-specific OS. These data evidence an association between specific CNVs in chromosomes B1, B4 and F2, and poor prognosis in FMCs.

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Section: Discussionmentioning

confidence: 99%

Analysis of Copy-Number Variations and Feline Mammary Carcinoma Survival

Granados-Soler

Bornemann-Kolatzki²,

Beck³

et al. 2020

Sci Rep

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“…In this work, we report the involvement of α-catenin, a molecular linker between AJs and cytoskeleton, in controlling CICs formation of human tumor cells. Alpha-catenin is well known as a tumor suppressor, whose inactivation by multiple mechanisms contributes to advanced phenotypes of various human tumors 24 25 26 . Multiple oncogenic pathways such as YAP and NF-κb signaling were found affected by α-catenin 27 28 , the growth of tumor cells was usually inhibited by α-catenin in cell-autonomous way, which was confirmed in our experiment (data not shown).…”

Section: Discussionmentioning

confidence: 99%

Impaired formation of homotypic cell-in-cell structures in human tumor cells lacking alpha-catenin expression

Wang

Ning

Chen³

et al. 2015

Sci Rep

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Although cell-in-cell structures (CICs) could be detected in a wide range of human tumors, homotypic CICs formed between tumor cells occur at low rate for most of them. We recently reported that tumor cells lacking expression of E- and P-cadherin were incapable of forming homotypic CICs by entosis, and re-expression of E- or P-cadherin was sufficient to induce CICs formation in these tumor cells. In this work, we found that homotypic CICs formation was impaired in some tumor cells expressing high level of E-cadherin due to loss expression of alpha-catenin (α-catenin), a molecular linker between cadherin-mediated adherens junctions and F-actin. Expression of α-catenin in these tumor cells restored cell-cell adhesion and promoted CICs formation in a ROCK kinase-dependent way. Thus, our work identified α-catenin as another molecule in addition to E- and P-cadherin that were targeted to inactivate homotypic CICs formation in human tumor cells.

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“…α-catenin, which bridges the E-cadherin-β catenin complex and actin cytoskeleton, is essential for maintaining the integrity of the intercellular adherens junction [7]. There are three forms of α-catenin: neural (N), epithelial (E) and testis/heart (T) [8].…”

Section: Introductionmentioning

confidence: 99%

Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells

Wang

Parrish

2015

Apoptosis

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The aging kidney undergoes structural and functional alterations which make it more susceptible to drug-induced acute kidney injury (AKI). Previous studies in our lab have shown that the expression of α(E)-catenin is decreased in aged kidney and loss of α(E)-catenin potentiates AKI-induced apoptosis, but not necrosis, in renal tubular epithelial cells (NRK-52E cells). However, the specific apoptotic pathway underlying the increased AKI-induced cell death is not yet understood. In this study, cells were challenged with nephrotoxicant cisplatin to induce AKI. A ~5.5-fold increase in Fas expression in C2 (stable α(E)-catenin knockdown) relative to NT3 (non-targeted control) cells was seen. Increased caspase-8 and -9 activation was induced by cisplatin in C2 as compared to NT3 cells. In addition, decreased Bcl-2 expression and increased BID cleavage and cytochrome C release were detected in C2 cells after cisplatin challenge. Treating the cells with cisplatin, in combination with a Bcl-2 inhibitor, decreased the viability of NT3 cells to the same level as C2 cells after cisplatin. Furthermore, caspase-3/-7 activation is blocked by Fas, caspase-8, caspase-9 and pan-caspase inhibitors. These inhibitors also completely abolished the difference in viability between NT3 and C2 cells in response to cisplatin. These results demonstrate a Fas-mediated apoptotic signaling pathway that is enhanced by the age-dependent loss of α(E)-catenin in renal tubule epithelial cells.

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α-catenin

Cited by 33 publications

References 60 publications

Analysis of Copy-Number Variations and Feline Mammary Carcinoma Survival

Analysis of Copy-Number Variations and Feline Mammary Carcinoma Survival

Impaired formation of homotypic cell-in-cell structures in human tumor cells lacking alpha-catenin expression

Loss of α(E)-catenin promotes Fas mediated apoptosis in tubular epithelial cells

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