Fig. 5: FAM126A overexpression suppresses the PI3K/AKT pathway and EMT through ENO1 downregulation. | Cell Death Discovery

Fig. 5: FAM126A overexpression suppresses the PI3K/AKT pathway and EMT through ENO1 downregulation.

From: FAM126A interacted with ENO1 mediates proliferation and metastasis in pancreatic cancer via PI3K/AKT signaling pathway

Fig. 5: FAM126A overexpression suppresses the PI3K/AKT pathway and EMT through ENO1 downregulation.The alternative text for this image may have been generated using AI.

A Proteins interacting with Girdin were examined in PANC‑1 and BxPC‑3 cells by co‑IP. Cell lysates were analyzed by Western blotting. B In immunofluorescence-based co-localization assays, FAM126A interacted with ENO1 in the cytoplasm. C Relative ENO1 expression levels assessed in PC tissues according to the GEPIA2 database. D Kaplan–Meier curves for disease-free survival and overall survival in PC based on the GEPIA2 database. E ENO1 levels were elevated in cells overexpressing FAM126A and decreased after FAM126A knockdown, while FAM126A levels were decreased after ENO1 knockdown, as determined by qRT-PCR and immunoblot. GAPDH was utilized for normalization. F–I ENO1 silencing dampened FAM126A overexpression-induced BxPC-3 cell proliferation, as measured by CCK-8, EdU, clonogenic, cell-cycle distribution assays. J–K ENO1 silencing dampened FAM126A overexpression-induced BxPC-3 cell proliferation, as measured by wound healing and transwell assays. L Downregulation of ENO1 in BXPC-3-FAM126A cells reversed the upregulation of N-cadherin, Vimentin, and Snail by FAM126A, and the downregulation of E-cadherin. M Phosphorylated PI3K and Akt amounts in PANC‑1 and BxPC‑3 cells were examined by immunoblot. *P < 0.05 **P < 0.01, ***P < 0.001.

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