ArticleMedical oncology (Northwood, London, England)2025
Combined inhibition of insulin growth factor 1 receptor and autophagy prevents colorectal cancer metastasis.
Article in Medical oncology (Northwood, London, England), 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Bidirectional Interactions Between Immune Regulation and the Insulin-like Growth Factor Axis in Colorectal Cancer.International journal of molecular sciences · 2026Review
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Authors and funding
16 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The role of Insulin-like growth factor 1 (IGF-1) in promoting cancer proliferation has been identified, yet its potential role in metastasis has not been fully elucidated. Autophagy plays a pivotal, yet controversial, role in regulating cancer cell behaviour. Our previous transcriptomic analysis identified autophagy-related genes and insulin-like growth factor 1 receptor (IGF-1R) among the most differentially expressed in advanced versus early-stage colorectal cancer (CRC). In this study, we investigated the functional interplay between IGF-1R signalling and autophagy in CRC progression and metastasis, using a panel of CRC cell lines, including HCT116 cells with targeted CRISPR-Cas9 knockout of ATG5 and ATG7. Our results demonstrate that stimulation with IGF-1 enhances autophagic flux, whereas IGF-1R knockdown suppresses autophagic activity. Notably, dual inhibition of IGF-1R and autophagy led to a marked reduction in CRC cell migration and invasion. In ATG5-/- and ATG7-/- cells, IGF-1R silencing significantly downregulated mesenchymal markers Vimentin, Slug, and Snail, while upregulating the epithelial marker E-cadherin. Additionally, combined inhibition resulted in increased size and number of focal adhesion molecules, such as paxillin and zyxin. Collectively, these findings highlight the synergistic effect of IGF-1R and autophagy inhibition in suppressing EMT and metastatic potential in CRC cells, suggesting that this combinatorial approach may represent a promising therapeutic strategy for metastatic CRC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.