ArticleHuman cell2025
Exosomal FGD5-AS1 promotes proliferation of lung cancer cells under hypoxia by inhibiting miR-1179 and activating P-cadherin.
Article in Human cell, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The trial behind it
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Who cites it
2 citing papers in PubMed.
- A multi-algorithm machine learning framework identifies FGD5, LRRC36, C8B, and MYOC as novel diagnostic biomarkers in lung adenocarcinoma.Discover oncology · 2026Article
- CDH3 in human tumors: tumor biology and potential therapeutic target.Frontiers in pharmacology · 2026Review
Corrections and comments
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Authors and funding
6 authors.
Funding
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Abstract
Lung adenocarcinoma (LUAD) continues to be a major contributor to cancer-related deaths due to its aggressive nature and resistance to current therapies, highlighting the need for novel molecular insights and therapeutic targets. This study investigated the function of exosomal lncRNA FGD5-AS1 in lung adenocarcinoma (LUAD) and its interaction with miR-1179 and CDH3. We discovered that FGD5-AS1 was substantially overexpressed in LUAD cells and exosomes under hypoxic conditions, while miR-1179, a tumor suppressor, directly targeted and downregulated CDH3. By sponging miR-1179, FGD5-AS1 serves as a competing endogenous RNA (ceRNA) to prevent the suppression of CDH3, thereby promoting LUAD cell growth, movement, and infiltration. It was demonstrated that knockdown of FGD5-AS1 or overexpression of miR-1179 significantly reduced tumor growth in vivo. These results demonstrate a novel exosome-mediated regulatory axis, suggesting that targeting the FGD5-AS1/miR-1179/CDH3 pathway could offer new therapeutic strategies for LUAD.
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Registered trials
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