FAT1 cadherin controls neuritogenesis during NTera2 cell differentiation

Ahmed, Abdulrzag F; Bock, Charles E. de; Sontag, Estelle; Hondermarck, Hubert; Lincz, Lisa F.; Thorne, Rick F.

doi:10.1016/j.bbrc.2019.04.197

Cited by 10 publications

(9 citation statements)

References 38 publications

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“…However, the molecular mechanisms of FAT1 in development of bladder cancer were not investigated in the present study. It has previously been demonstrated that FAT1 is involved in regulating the Hippo pathway ( 34 , 35 ), the Wnt/β-catenin pathway ( 36 ) and the MAPK/ERK pathway ( 37 ); however, whether these pathways are regulated in BC via FAT1 warrants further investigation. Moreover, the function of FAT1 in BC was not examined by an in vivo assay in the present study.…”

Section: Discussionmentioning

confidence: 99%

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Wang

Liu

2020

Int J Mol Med

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FAT atypical cadherin 1 (FAT1) regulates complex mechanisms for the promotion of oncogenesis or the suppression of malignancies. Sulforaphane (SFN) has antioxidant and anti-tumor activities. The present study investigated the roles of SFN and FAT1 in bladder cancer (Bc). The expression of FAT1 in Bc cell lines and tissues was measured by western blot analysis and reverse transcription-quantitative PcR (RT-qPcR). The association between FAT1 expression and the 5-year survival rate of patients with Bc was evaluated. The viability of and FAT1 expression in T24 and SW780 cells exposed to various concentrations of SFN were detected by MTT assay, and western blot analysis and RT-qPcR, respectively. Furthermore, the viability, migration, invasion and apoptosis of and FAT1 expression in Bc cells subjected to FAT1 overexpression or knockdown, and with or without SFN stimulation, were examined. The results revealed that FAT1 expression in Bc cells and tissues was increased, and patients with a high FAT-1 expression had a shorter 5-year survival time than those with a low FAT-1 expression. Bc cell viability and FAT1 expression were suppressed by SFN in a concentration-dependent manner. The knockdown of FAT1 inhibited the viability, migration and invasion, and promoted the apoptosis of Bc cells, whereas the overexpression of FAT1 produced opposite effects. In addition, cells exposed to SFN exhibited a reduced viability, migration, invasion and an increased apoptosis, effects which were promoted by FAT1 knockdown; however, the overexpression of FAT1 blocked the above-mentioned effects of SFN on the cells. On the whole, the present study demonstrates that SFN suppresses the progression of Bc by inhibiting the expression of FAT-1; thus, SFN may be used as a potential drug for the treatment of Bc.

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Section: Discussionmentioning

confidence: 99%

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Wang

Liu

2020

Int J Mol Med

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“…Cadherins can be classified into several subtypes: type I classical cadherins such as E-cadherin, N-cadherin, and P-cadherin; type II classical cadherins such as VE-cadherin (CDH5) and OB-cadherin (CDH11) (9, 10); the desmosomal cadherins (11, 12); the seven-pass transmembrane cadherins (13, 14); FAT and dachsous (DCHS) group cadherins (15–17); and protocadherins (PCDHs) (18–21) (Table 1). Nearly all cadherins are transmembrane proteins with three components: (1) an extracellular cadherin domain (EC) responsible for homotypic cadherin-cadherin interaction; (2) a single-pass transmembrane domain (absent in seven-pass transmembrane cadherins); and (3) a cytoplasmic domain acts as a connector between cell surface and cytokeleton (21, 29) (Figure 1).…”

Section: Types Of Cadherinmentioning

confidence: 99%

Cadherin Signaling in Cancer: Its Functions and Role as a Therapeutic Target

et al. 2019

Front. Oncol.

154

118

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Cadherin family includes lists of transmembrane glycoproteins which mediate calcium-dependent cell-cell adhesion. Cadherin-mediated adhesion regulates cell growth and differentiation throughout life. Through the establishment of the cadherin-catenin complex, cadherins provide normal cell-cell adhesion and maintain homeostatic tissue architecture. In the process of cell recognition and adhesion, cadherins act as vital participators. As results, the disruption of cadherin signaling has significant implications on tumor formation and progression. Altered cadherin expression plays a vital role in tumorigenesis, tumor progression, angiogenesis, and tumor immune response. Based on ongoing research into the role of cadherin signaling in malignant tumors, cadherins are now being considered as potential targets for cancer therapies. This review will demonstrate the mechanisms of cadherin involvement in tumor progression, and consider the clinical significance of cadherins as therapeutic targets.

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“…Similar to Drosophila Ft, the FAT1 protein has been shown to be an upstream factor of the Hippo signaling pathway (20). FAT1 acts as an upstream regulator of TAZ, as well as an upstream regulator of YAP in the process of neuronal differentiation (56). The intracellular domain of FAT1 interacts with a multimeric Hippo signaling protein and participates in its assembly, which in turn induces the kinase Tao to activate the Hippo kinase cassette (17).…”

Section: Signaling Pathways and Mechanismsmentioning

confidence: 99%

Role of FAT1 in health and disease (Review)

2021

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FAT atypical cadherin 1 (FAT1), which encodes a protocadherin, is one of the most frequently mutated genes in human cancer. Over the past 20 years, the role of FAT1 in tissue growth and in the development of diseases has been extensively studied. There is definitive evidence that FAT1 serves a substantial role in the maintenance of organs and development, and its expression appears to be tissue-specific. FAT1 activates a variety of signaling pathways through protein-protein interactions, including the Wnt/β-catenin, Hippo and MAPK/ERK signaling pathways, which affect cell proliferation, migration and invasion. Abnormal FAT1 expression may lead to the development of tumors and may affect prognosis. Therefore, FAT1 may have potential in tumor therapy. The structural and functional changes mediated by FAT1, its tissue distribution and changes in FAT1 expression in human diseases are described in the present review, which provides further insight for understanding the role of FAT1 in development and disease. Contents 1. Introduction 2. Signaling pathways and mechanisms 3. FAT1 in development 4. FAT1 in hereditary diseases 5. FAT1 in cancer 6. Therapeutic targeting of FAT1 7. Conclusions and perspectives

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FAT1 cadherin controls neuritogenesis during NTera2 cell differentiation

Cited by 10 publications

References 38 publications

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Sulforaphane suppresses the viability and metastasis, and promotes the apoptosis of bladder cancer cells by inhibiting the expression of FAT‑1

Cadherin Signaling in Cancer: Its Functions and Role as a Therapeutic Target

Role of FAT1 in health and disease (Review)

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