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Published on: August 2, 2024
PLIN1 restoration modulates lipid reprogramming and impedes tumor growth in ovarian cancer
Qing Liu1, Minzhi Sun2,3, Wenyan Wang4
1Department of Obstetrics and Gynecology, The Second Affiliated Hospital of Anhui Medical University, No.678 Furong Road, Economic Development Zone, Hefei, Anhui, China.
Background:
Ovarian cancer (OC) is an aggressive gynecologic malignancy characterized by remarkable metabolic reprogramming. Lipid metabolic remodeling is closely associated with malignant proliferation, metastasis, and therapeutic resistance, but key regulators remain incompletely understood.
Methods:
Integrated lipid metabolomics and transcriptome sequencing analyses were performed using paired OC and adjacent non-tumor tissues. Differential lipids (VIP > 1.5 and false discovery rate [FDR]-adjusted P < 0.05) and differentially expressed genes (|log2FC| > 1 and FDR-adjusted P < 0.05) were screened and integrated with lipid metabolism-related gene sets. PLIN1 expression and function were further evaluated in clinical samples, OC cell lines, and xenograft models.
Results:
Perilipin 1 (PLIN1) was identified as a candidate lipid metabolism-related hub gene with previously underexplored roles in OC. PLIN1 was downregulated in clinical OC specimens and OC cell lines. PLIN1 expression was negatively associated with carnitine palmitoyltransferase 1 A (CPT1A), and positively associated with acyl-CoA synthetase long-chain family member 3 (ACSL3), acetyl-CoA carboxylase 1 (ACC1), fatty acid synthase (FASN), and stearoyl-CoA desaturase 1 (SCD1). Functionally, PLIN1 overexpression suppressed cell viability, migration, and invasion; promoted intracellular lipid accumulation and lipid droplet formation; increased several lipid storage/lipogenesis-associated enzymes; and decreased CPT1A expression. In vivo, PLIN1 overexpression inhibited xenograft tumor growth, enhanced lipid deposition, reduced Ki67 expression, and was accompanied by decreased HSL, ATGL, and p-CREB expression.
Conclusions:
These findings suggest that PLIN1 may suppress OC progression, at least in part, by reshaping lipid storage and lipolysis-related metabolic signaling. Further studies are required to define the direct regulatory mechanisms and validate its clinical utility.
Insights
Perilipin 1 (PLIN1) suppresses ovarian cancer (OC) progression by altering lipid metabolism. Downregulation of PLIN1 in OC suggests it may be a therapeutic target for this aggressive gynecologic malignancy.
Area of Science:
- Oncology
- Metabolomics
- Molecular Biology
Background:
- Ovarian cancer (OC) exhibits significant metabolic reprogramming, particularly in lipid metabolism, which is linked to its progression and treatment resistance.
- Key regulators of lipid metabolism in OC remain poorly understood, hindering the development of targeted therapies.
Purpose of the Study:
- To identify key regulators of lipid metabolism in ovarian cancer.
- To investigate the role of Perilipin 1 (PLIN1) in OC progression and its associated metabolic pathways.
Main Methods:
- Integrated analysis of lipid metabolomics and transcriptome sequencing in OC and adjacent non-tumor tissues.
- Screening of differential lipids and genes, followed by integration with lipid metabolism gene sets.
- Evaluation of PLIN1 expression and function in clinical samples, cell lines, and xenograft models.
Main Results:
- Perilipin 1 (PLIN1) was identified as a downregulated hub gene in OC tissues and cell lines.
- PLIN1 overexpression suppressed OC cell viability, migration, and invasion, while promoting lipid accumulation and lipogenesis.
- In vivo studies showed that PLIN1 overexpression inhibited tumor growth and altered lipid metabolism-related signaling pathways.
Conclusions:
- PLIN1 plays a suppressive role in ovarian cancer progression, likely through modulation of lipid storage and lipolysis.
- PLIN1 represents a potential therapeutic target for ovarian cancer, warranting further investigation into its regulatory mechanisms and clinical utility.
