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

Yu, Wenbin; Li, Yang; Li, Ting; Zhang, Yi

doi:10.3389/fonc.2019.00989

Cited by 155 publications

(143 citation statements)

References 214 publications

Supporting

Mentioning

118

Contrasting

Unclassified

Order By: Relevance

“…On the contrary, they promote the generation of T regs [116]. Accordingly, it was found that in DCs β-catenin, an important transcription factor downstream E-cadherin signaling pathway [117], is essential for the expression of immunosuppressive mediators and for the stimulation of T regs and the concomitant suppression of effector T cells [118]. Moreover, it has also been proposed that dendritic cells may contribute to sustaining an immunosuppressive tumor microenvironment after up-regulation of E-cadherin on their membrane, a phenomenon triggered by soluble factors secreted by tumor cells [119].…”

Section: E-cadherin and The Immune Systemmentioning

confidence: 99%

E-Cadherin in Pancreatic Ductal Adenocarcinoma: A Multifaceted Actor during EMT

Sommariva

Gagliano

2020

Cells

View full text Add to dashboard Cite

Epithelial-to-mesenchymal transition (EMT) is a step-wise process observed in normal and tumor cells leading to a switch from epithelial to mesenchymal phenotype. In tumors, EMT provides cancer cells with a metastatic phenotype characterized by E-cadherin down-regulation, cytoskeleton reorganization, motile and invasive potential. E-cadherin down-regulation is known as a key event during EMT. However, E-cadherin expression can be influenced by the different experimental settings and environmental stimuli so that the paradigm of EMT based on the loss of E-cadherin determining tumor cell behavior and fate often becomes an open question. In this review, we aimed at focusing on some critical points in order to improve the knowledge of the dynamic role of epithelial cells plasticity in EMT and, specifically, address the role of E-cadherin as a marker for the EMT axis.

show abstract

Section: E-cadherin and The Immune Systemmentioning

confidence: 99%

E-Cadherin in Pancreatic Ductal Adenocarcinoma: A Multifaceted Actor during EMT

Sommariva

Gagliano

2020

Cells

View full text Add to dashboard Cite

show abstract

“…The process which enables tumor cells to achieve migration and invasion is called epithelial-mesenchymal transition (EMT) and represents a driving force in tumorigenesis [23]. In the course of EMT, essential proteins for epithelial cell-cell adhesion, such as E-cadherin, are downregulated, thus weakening epithelial tissue integrity and polarization of epithelial cell layers [24]. Under normal circumstances, detached epithelial cells undergo apoptosis, a phenomenon termed anoikis.…”

Section: Introductionmentioning

confidence: 99%

Dexamethasone Inhibits Spheroid Formation of Thyroid Cancer Cells Exposed to Simulated Microgravity

Melnik

Sahana

Corydon

et al. 2020

Cells

View full text Add to dashboard Cite

Detachment and the formation of spheroids under microgravity conditions can be observed with various types of intrinsically adherent human cells. In particular, for cancer cells this process mimics metastasis and may provide insights into cancer biology and progression that can be used to identify new drug/target combinations for future therapies. By using the synthetic glucocorticoid dexamethasone (DEX), we were able to suppress spheroid formation in a culture of follicular thyroid cancer (FTC)-133 cells that were exposed to altered gravity conditions on a random positioning machine. DEX inhibited the growth of three-dimensional cell aggregates in a dose-dependent manner. In the first approach, we analyzed the expression of several factors that are known to be involved in key processes of cancer progression such as autocrine signaling, proliferation, epithelial–mesenchymal transition, and anoikis. Wnt/β-catenin signaling and expression patterns of important genes in cancer cell growth and survival, which were further suggested to play a role in three-dimensional aggregation, such as NFKB2, VEGFA, CTGF, CAV1, BCL2(L1), or SNAI1, were clearly affected by DEX. Our data suggest the presence of a more complex regulation network of tumor spheroid formation involving additional signal pathways or individual key players that are also influenced by DEX.

show abstract

“…Vimentin, a mesenchymal-specific IFs protein, is a distinct feature of EMT [53]. The EMT activation is correlated with molecular changes as shifts in cadherins expression [54], cytokeratin loss, vimentin and collagen increased expressions [53,55]. Moreover, PI3K-AKT pathway are essential to maintain the CSC-like phenotype and EMT characteristics in breast cancer cells [56].…”

Section: Discussionmentioning

confidence: 99%

Sevoflurane Modulates Akt Isoforms In Triple Negative Breast Cancer Cell Line

Tiron

Postu

Vacarean-Trandafir

et al. 2020

Preprint

View full text Add to dashboard Cite

Background: Triple negative breast cancer (TNBC) is a highly aggressive tumor, associated with high rates of early distant recurrence and short survival times and treatment may require surgery, and thus anesthesia. The effects of anesthetic drugs on cancer progression are under scrutiny, but published data are controversial and the involved mechanisms unclear. Anesthetic agents have been shown to modulate several molecular cascades, including PI3K/AKT/mTOR. AKT isoforms are frequently amplified in various malignant tumors and associated with malignant cell survival, proliferation and invasion. Their activation is often observed in human cancers and is associated with decreased survival rate. Certain anesthetics are known to affect hypoxia cell signalling mechanisms by upregulating hypoxia-inducible factors (HIFs). Methods: MCF-10A and MDA-MB 231 cells were cultivated and CellTiter-Blue® Cell Viability assay, 2D and 3D matrigel assay, immunofluorescence assays and gene expressions were performed after exposure to different sevoflurane concentrations.Results: Sevoflurane exposure of triple negative breast cancer cells results in morphological and behavioral changes. Sevoflurane differently influences the AKT isoforms expression in a time-dependent manner, with an important early AKT3 upregulation. The most significant effects occur at 72 hours after 2mM sevoflurane treatment and consist in increased viability, proliferation and aggressiveness and increased vimentin and HIF expression. Conclusion: Sevoflurane exposure during surgery may contribute to cancer recurrence via AKT3 induced EMT and by all three AKT isoforms enhanced cancer cell survival and proliferation.

show abstract

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

Cited by 155 publications

References 214 publications

E-Cadherin in Pancreatic Ductal Adenocarcinoma: A Multifaceted Actor during EMT

E-Cadherin in Pancreatic Ductal Adenocarcinoma: A Multifaceted Actor during EMT

Dexamethasone Inhibits Spheroid Formation of Thyroid Cancer Cells Exposed to Simulated Microgravity

Sevoflurane Modulates Akt Isoforms In Triple Negative Breast Cancer Cell Line

Contact Info

Product

Resources

About