Abstract
Epithelial-to-Mesenchymal Transition (EMT) has been shown to be crucial in tumorigenesis where the EMT program enhances metastasis, chemoresistance and tumor stemness. Due to its emerging role as a pivotal driver of tumorigenesis, targeting EMT is of great therapeutic interest in counteracting metastasis and chemoresistance in cancer patients. The hallmark of EMT is the upregulation of N-cadherin followed by the downregulation of E-cadherin, and this process is regulated by a complex network of signaling pathways and transcription factors. In this review, we summarized the recent understanding of the roles of E- and N-cadherins in cancer invasion and metastasis as well as the crosstalk with other signaling pathways involved in EMT. We also highlighted a few natural compounds with potential anti-EMT property and outlined the future directions in the development of novel intervention in human cancer treatments. We have reviewed 287 published papers related to this topic and identified some of the challenges faced in translating the discovery work from bench to bedside.
Highlights
Cadherins were originally identified by Takeichi as cell surface molecules involved inCa2+ -dependent adhesion mechanism in Chinese hamster V79 cells [1]
Extrinsic apoptosis pathway is initiated by death receptors which are members of tumor necrosis factors (TNFs) that are capable of regulating cell fate [73]
Homophilic interaction of the E-cadherin resulted in an increased Rac1 and cell division control protein 42 homolog (Cdc42) protein expression, which was primarily responsible for STAT3 activation (Figure 3)
Summary
Cadherins were originally identified by Takeichi as cell surface molecules involved in. Previous studies showed that the anchoring of the formation of adaptive cell–cell contacts in response to mechanical stress, long-range cell–cell cadherin complexes to F-actin mediated by vinculin can restore E-cadherin-dependent cell contacts interactions and tissue-scale mechanics [11]. The cadherin–catenin adhesion is the complexes to F-actin mediated by vinculin can restore E-cadherin-dependent cell contacts without essential component of adherens junctions that maintain tissue stability and dynamic cell movements the presence of α-catenin actin binding domain [14]. E-cadherin is highly expressed in ovarian cancer patients where soluble E-cadherin is released in the form of exosomes to promote tumor angiogenesis via activation of β-catenin and NF-κB signaling [45].
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