Metastatic pancreatic adenocarcinoma is driven by cancer stem cells, formation and upregulation of the premetastatic/metastatic niche, EMT, and the largely hypoxic state of the tumor microenvironment (TME). These characteristics of metastasis feed into each other continuously to further the development and distribution of the cancer. Cancer stem cells serve as the central driver of metastasis due to their inherent plasticities and contribute to chemoresistance, functioning of the premetastatic niche, and induction of EMT (Sancho et al. 2016). In the premetastatic niche, extracellular signaling contributes to a TME that facilitates the development of the cancer. EMT allows cancer cells to detach from a tumor site and relocalize, as well as change their phenotype to a less differentiated state. When tumor growth reaches a critical point, cancerous cells deprive their environments of oxygen, leading to hypoxia and potential metabolic shifts such as the Warburg effect or oxidative phosphorylation (Sancho et al. 2016).
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