Fig. 3: PLEKHA1-TACC2 promotes VM formation via activating the EphA2/AKT/MMP2 signalling pathway. | Cell Death & Differentiation

Fig. 3: PLEKHA1-TACC2 promotes VM formation via activating the EphA2/AKT/MMP2 signalling pathway.

From: The PLEKHA1-TACC2 fusion gene drives tumorigenesis via vascular mimicry formation in esophageal squamous-cell carcinoma

Fig. 3

A The lysates of KYSE30 cells stably expressing Flag-tagged PLEKHA1, TACC2, Pe4Te20, Pe11Te17, Pe10Te23, Pe5Te17, Pe2Te23, or an empty vector were blotted for total EphA2, p-EphA2 (S897), total AKT, and p-AKT (S473). B The VM ability of KYSE30 cells stably expressing Flag-tagged PLEKHA1, TACC2, Pe4Te20, Pe11Te17, Pe10Te23, Pe5Te17, Pe2Te23, or an empty vector was measured by an in vitro tube formation assay. C The conditioned medium of KYSE30 cells stably expressing Flag-tagged PLEKHA1, TACC2, Pe4Te20, Pe11Te17, Pe10Te23, Pe5Te17, Pe2Te23, or an empty vector was collected for gelatin zymography (top), and the cell lysates were blotted for β-Actin (bottom). D–F Representative images of VM in tumor tissues obtained from athymic nude mice bearing KYSE30 (left) or KYSE150 (right) tumors (D), ESCC patients (E), and PDX grown in mice (F). Red arrows: the tubule-like VM channels. Blue arrows: the blood vessels lined by CD31-positive endothelial cells. Scale bars were indicated in the images.

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