Fig. 8: Proposed model of homophilic ATP1A1 interactions trigger activin A secretion to promote EMT of tumor cells and myofibroblast activation for tumor invasion and metastasis. | Nature Communications

Fig. 8: Proposed model of homophilic ATP1A1 interactions trigger activin A secretion to promote EMT of tumor cells and myofibroblast activation for tumor invasion and metastasis.

From: Homophilic ATP1A1 binding induces activin A secretion to promote EMT of tumor cells and myofibroblast activation

Fig. 8

Homophilic ATP1A1 interactions between ATP1A1-overexpressing tumor cells and fibroblasts stabilize ATP1A1 on fibroblasts leading to calcium oscillations, NF-κB activation, and activin A secretion. High concentration of activin A along tumor-stromal interface induces EMT of tumor cells for tumor invasion and metastasis. On the other hand, autocrine activin A activates a subpopulation of peri-tumoral αSMA+ myofibroblast.

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