The epithelial to mesenchymal transition (EMT) allows cancer cells to begin the process of metastasis by unadhering to one tissue and migrating to another location. A major characteristic of this process is the loss of e-cadherin, which can result from the expression of multiple transcription factors including SNAIL, ZEB, and KLF8. EMT can also be induced by certain growth factor pathways as well as TGF beta and hypoxia. The researchers aim to target these transcription factors and signaling pathways as well as the hypoxic tumor microenvironment in order to prevent metastasis from occurring. If cancerous cells are unable to carry out EMT, the effects of metastasis should lessen. Subsequently, apoptosis-inducing therapy can be delivered to these now stationary cells. A region of interest for the researchers is aptamer-regulated exosomal therapy, where aptamers can serve as binding partners for these transcription factors and elements in these signaling pathways. This binding can inhibit the downstream effects, such as the induction of EMT. A cell suicide gene or cytokine such as TRAIL may also be incorporated into the interior of the exosome for targeted delivery.
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