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1,3,6-Tri-O-Galloyl-α-D-Glucosa Sintético Imita el Inhibidor de la Vía Hippo VT107 en la Supresión de la Inflamación

Angélique Sabaoth Konan¹, Rosalie Zilinski¹, Mirolla Tadrous¹

¹Laboratoire d'Oncologie Moléculaire, Chaire en Prévention et Traitement du Cancer, Université du Québec à Montréal, Montréal, QC, H3C 3P8, Canada.

Journal of inflammation research

|December 25, 2025

Abstracto

Background:

Glioblastoma (GBM) is the most aggressive primary tumor of the adult central nervous system, not only characterized by rapid proliferation and diffuse brain infiltration but also by a pronounced pro-inflammatory microenvironment that fuels tumor progression and therapeutic resistance. Current standard-of-care, surgical resection followed by radiotherapy and chemotherapy, offers limited survival benefit, partly due to inflammation-driven invasion and immune evasion. The Hippo signaling pathway, a critical regulator of cell proliferation, apoptosis, and tissue homeostasis, has recently been implicated in inflammatory signaling, making it an attractive therapeutic target.

Purpose:

In this study, we investigated the anti-inflammatory and anti-invasive properties of 1,3,6-tri-O-galloyl-α-D-glucose (αTGG), the α-anomer of βTGG from Terminalia chebula, in comparison with pharmacological Hippo pathway inhibitors IAG933, VT107, and GNE7883.

Results:

To mimic the inflammatory milieu associated with GBM, U87 cells were treated with Concanavalin A (ConA), which induced phosphorylation of ERK and IκB, key mediators of MAPK and NF-κB inflammatory pathways. Both αTGG and Hippo pathway inhibitors effectively suppressed these phosphorylation events, with VT107 showing the strongest effect. ConA exposure downregulated Hippo pathway downstream effectors (AXL, CTGF, CYR61) in a TEAD-dependent manner, highlighting the interplay between Hippo signaling and inflammatory transcriptional control. Importantly, αTGG and VT107 also significantly attenuated ConA-induced activation of proMMP-2 to MMP-2 and reduced the expression of multiple pro-inflammatory mediators, including COX2, CCL22, CCR2, CCR4, CXCL10, CXCL12, CXCR1, FASLG, IFNG, IL13, and IL17A.

Conclusion:

These findings underscore the dual anti-inflammatory and anti-invasive actions of αTGG, positioning it as a promising candidate for targeting inflammation-driven GBM progression through modulation of Hippo pathway activity.

Palabras clave:

1,3,6-tri-O-galloyl-α-D-glucose Concanavalin A glioblastoma hippo pathway inhibitors inflammation

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