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Background <p>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.</p> Methods <p>Integrated lipid metabolomics and transcriptome sequencing analyses were performed using paired OC and adjacent non-tumor tissues. Differential lipids (VIP &gt; 1.5 and false discovery rate [FDR]-adjusted <i>P</i> &lt; 0.05) and differentially expressed genes (|log2FC| &gt; 1 and FDR-adjusted <i>P</i> &lt; 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.</p> Results <p>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&#xa0;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.</p> Conclusions <p>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.</p>

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PLIN1 restoration modulates lipid reprogramming and impedes tumor growth in ovarian cancer

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月7日

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  • Qing Liu,
  • Minzhi Sun,
  • Wenyan Wang

摘要

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.