Additional file 2 of Targeting of a novel interplay between MET tyrosine kinase and NRF2 enhances sensitivity to Paclitaxel in triple negative breast cancer

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Authors: I Taddei, Claudia Cirotti, Fabienne Lamballe, Olivier Castellanet, Flavio Maina, Vanessa Medici, Fabrizio Fierro, Giacomo Corleone, Francesca De Nicola, Maurizio Fanciulli, Eleonora Cesari, Alba Di Leone
+5 more Alessia Piermattei, Angela Santoro, Chiara Naro, Claudio Sette, Daniela Barilà
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Abstract

Supplementary Material 2. Figure S2 A) Immunoblotting analysis of pY1068EGFR, EGFR, pY1234/35MET and MET in MGT-13 cells after 16 h of PHA treatment. Actin was used as a loading control. Immunoblotting (B) and relative densitometric analyses (C) of MET, NRF2, HO-1 and p62 in MGT-13 cells transiently silenced for MET expression (siMET). Actin was used as a loading control. D) Immunofluorescence (left) and relative quantification analysis (right) of NRF2 (red) nuclear intensity in MGT-13 cells transiently silenced for MET expression (siMET). DNA (Hoechst, blue). E) RT-qPCR of NRF2 target genes in MGT-13 cells transiently silenced for MET expression (siMET). Actin was used as housekeeping gene. F) Immunoblotting analysis of pY1234/35MET and MET in MGT-13 cells after 24 h of PHA treatment. Actin was used as a loading control. G) PCA based on RNA-seq data for PHA and CTRL in MGT-13 cells. H) Volcano plot. Dots in blue are downregulated genes upon PHA treatment (log2Fold Change < -0.7 and p-value 0.7 and p-value 0.7 and p-value

Fields of Study & Subjects

Genomics phytochemicals and oxidative stress Breast Cancer Treatment Studies Cancer Mechanisms and Therapy

Publication details

Journal / source
Figshare
Publication date
1 January 2026
Language
EN