ArticleiScience2024
Reprogramming of fibroblasts into cancer-associated fibroblasts via IGF2-mediated autophagy promotes metastasis of lung cancer cells.
Article in iScience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Targeting lysosome-dependent cell death in cancer: towards therapeutic strategies.Biomarker research · 2026Review
- Convergent Microenvironment Linking Idiopathic Pulmonary Fibrosis and Lung Cancer.Expert reviews in molecular medicine · 2026Review
- Advances in understanding the tumor microenvironment of neuroendocrine prostate cancer.Frontiers in oncology · 2026Review
- Proteome changes associated with effect of high dose single-fractionation radiation on lung adenocarcinoma cell lines.Scientific reports · 2025Article
- Lactate-mediated metabolic reprogramming of tumor-associated macrophages: implications for tumor progression and therapeutic potential.Frontiers in immunology · 2025Review
- Autophagy stimulation influenced the angiogenesis and metastasis behavior of human triple-negative breast cancer cells.BioImpacts : BI · 2025Article
Corrections and comments
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Authors and funding
11 authors.
Funding
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Abstract
Cancer-associated fibroblasts (CAFs) are major component of stromal cells. Growing evidence suggests that CAFs promote tumor growth and metastasis; however, the reprogramming of normal fibroblasts (NFs) into CAFs by tumor cells still remains largely unknown. In this study, we found that non-small cell lung cancer (NSCLC) cells activated NFs into CAFs via autophagy induction. Insulin-like growth factor 2 (IGF2) secreted by NSCLC cells mediated NSCLC cells' effect on autophagy induction and CAFs activation. Importantly, the activated CAFs promoted NSCLC cells growth, migration, and invasion. Further study showed that the activated CAFs facilitated NSCLC cells invasion via promoting epithelial-mesenchymal transition (EMT) process, upregulating metastasis-related genes, releasing CXCL12, and activating its downstream AKT serine/threonine kinase 1 (AKT)/ nuclear factor κB (NF-κB) signaling pathway. These findings revealed that IGF2-mediated autophagy plays a critical role in CAFs activation and suggested the IGF2-autophagy cascade in fibroblasts could be a potential target for lung cancer therapy.
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Registered trials
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