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Fig. 5 | Biological Research

Fig. 5

From: Galectins in epithelial-mesenchymal transition: roles and mechanisms contributing to tissue repair, fibrosis and cancer metastasis

Fig. 5

Gal-1 pathways promoting EMT in cancer. (a) Gal-1 promotes EMT in gastric cancer cells through a TGFR-β/Smad pathway and can be blocked with the Gal-1 inhibitor ITD1. (b) Gal-1 secreted from gastric cancer cells or CAFs induces EMT through a mechanism involving β1-integrin and Gli-1. (c) Overexpression of Gal-1 in gastric cancer cells increases the levels of S1PR1 at the cell surface, which is required for Gal-1-induced EMT through an unknown pathway. (d) Overexpression of Gal-1 in ovarian cancer cells activates MAPK JNK/p38 signaling through an unknown mechanism promoting EMT. (e) Activation of TLR-4 induces Gal-1 via PI3K/AKT or ERK-AKT pathways leading to EMT. (f) Gal-1 overexpression in HCC cells induces EMT through a Integrin/FAK/PI3K/AKT pathway. (g-j) Examples of extracellular Gal-1 contribution to EMT, involving Ras/Rac1/MEKK4/JNK/AP (g) and FAK/PI3K/AKT/mTOR (h) in urothelial cancer cells, activation of NFkB signaling in pancreatic cancer cells (i) and activation of β -catenin pathway in colorectal cancer (j)

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Biological Research

ISSN: 0717-6287

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