ArticleThe American journal of pathology2025
Perilipin 2 Mediates Progression of Lung Adenocarcinoma by Modulating Lipid Metabolism.
Article in The American journal of pathology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Lipid Accumulation Promotes Tumorigenic Behaviour of Colorectal Cancer Cells.Journal of cellular and molecular medicine · 2026Article
- pH-responsive Folate-PEG modified ZIF-8 Nanoparticles deliver fisetin to Aquaporin-3 for cervical cancer therapy.iScience · 2026Article
- Lipid droplet-mitochondria contact sites as druggable spatial-pharmacology targets in respiratory disease: cross-cell-type mechanisms and translational strategies.Frontiers in cell and developmental biology · 2026Review
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Authors and funding
9 authors.
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Abstract
Perilipin 2 expression is related to poor prognosis of patients with various malignant tumors. It exists on the surface of lipid droplets (LDs), which store lipids that can be used as an energy source during cancer progression. However, the underlying mechanism of lipid metabolism involving LDs in the progression of lung adenocarcinoma is unclear. This study investigated the role of perilipin 2 in the regulation of lipid metabolism in lung adenocarcinoma, as well as patient prognosis. In clinicopathologic analyses, high perilipin 2 expression in adenocarcinomas was significantly associated with poor differentiation, blood vessel and pleural invasion, advanced cancer stage, and large tumor size relative to perilipin 2-negative cases. Furthermore, patients with high perilipin 2 expression had significantly shorter recurrence-free survival times. LD accumulation was significantly reduced in A549 and PC-9 lung adenocarcinoma cells with clustered regularly interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9) genome editing-mediated knockout of PLIN2 expression. Treatment of these cells with extracellular oleic acid induced accumulation of LDs, but the total amount of accumulated LDs was low in PLIN2 knockout cells compared with control cells. Cell proliferation and migration ability was also significantly reduced in PLIN2 knockout cells. Together, these results suggest that perilipin 2 mediates aggressive cancer progression in lung adenocarcinoma by regulating LD accumulation, and thus may represent a potential target for suppressing lung adenocarcinoma.
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