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- Academic Editor
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†These authors contributed equally.
Background: Gynecological malignancies, such as endometrial cancer (EC)
and uterine cancer are prevalent. Increased Acyl-CoA synthetase long-chain family
member 1 (ACSL1) activity may contribute to aberrant lipid metabolism, which is a
potential factor that contributes to the pathogenesis of endometrial cancer. This
study aimed to elucidate the potential molecular mechanisms by which ACSL1 is
involved in lipid metabolism in endometrial cancer, providing valuable insights
for targeted therapeutic strategies. Methods: Xenograft mouse models
were used to assess the effect of ACSL1 on the regulation of endometrial cancer
progression. ACSL1 protein levels were assessed via immunohistochemistry and
immunoblotting analysis. To assess the migratory potential of Ishikawa cells,
wound-healing and Transwell invasion assays were performed. Changes in lipids in
serum samples from mice with endometrial cancer xenotransplants were examined in
an untargeted lipidomic study that combined multivariate statistical methods with
liquid chromatography‒mass spectrometry (LC/MS). Results: Patient sample
and tissue microarray data suggested that higher ACSL1 expression is strongly
associated with the malignant progression of EC. Overexpression of ACSL1 enhances
fatty acid