150P Spatial pharmacoproteomics analysis of patient-derived tumoroids from colorectal cancer to identify new predictive biomarkers

Results: Mic60 silencing led to significant upregulation of EMT-associated transcription factors, including Zeb2, Lbx1, Snail, Twist1, accompanied by increased Ncadherin and Vimentin expression and decreased E-cadherin levels.NF-B signaling was also activated upon Mic60 loss.In vivo, Mic60 depletion resulted in faster tumor growth and increased tumor weight, indicating a pronounced effect on tumor aggressiveness.Conclusions: These findings demonstrate that Mic60 loss drives a more aggressive breast cancer phenotype, characterized by activation of EMT-and NF-B-related pathways, increased migratory and invasive potential, and accelerated tumor growth in vivo.Mic60 loss thus acts as a key driver of BC aggressiveness and highlights Mic60-associated pathways as potential targets for prognostic and therapeutic strategies in aggressive BC.

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Publication Details

Journal
ESMO Open
Published
2026-04-01
DOI
https://doi.org/10.1016/j.esmoop.2026.106293
Primary Topic
Cancer Cells and Metastasis
Type
article
Field-Weighted Citation Impact
0.00
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article

150P Spatial pharmacoproteomics analysis of patient-derived tumoroids from colorectal cancer to identify new predictive biomarkers

Katja Välimäki, Teijo Pellinen, AH Ree, J. Bruun et al.
ESMO Open
Cancer Cells and Metastasis
article

150P Spatial pharmacoproteomics analysis of patient-derived tumoroids from colorectal cancer to identify new predictive biomarkers

Katja Välimäki, Teijo Pellinen, AH Ree, J. Bruun, P. Eide, S. Meltzer, K. Augestad, N. Pasquier, C. Andreassen
article en

Abstract

Results: Mic60 silencing led to significant upregulation of EMT-associated transcription factors, including Zeb2, Lbx1, Snail, Twist1, accompanied by increased Ncadherin and Vimentin expression and decreased E-cadherin levels.NF-B signaling was also activated upon Mic60 loss.In vivo, Mic60 depletion resulted in faster tumor growth and increased tumor weight, indicating a pronounced effect on tumor aggressiveness.Conclusions: These findings demonstrate that Mic60 loss drives a more aggressive breast cancer phenotype, characterized by activation of EMT-and NF-B-related pathways, increased migratory and invasive potential, and accelerated tumor growth in vivo.Mic60 loss thus acts as a key driver of BC aggressiveness and highlights Mic60-associated pathways as potential targets for prognostic and therapeutic strategies in aggressive BC.

ESMO OpenVol. 11
University of Helsinki (FI), Akershus University Hospital (NO), Institute for Molecular Medicine Finland (FI)
Good health and well-being
Openalex Percentile: Top 12%
Cancer Cells and Metastasis
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