ArticleLipids in health and disease2024
SEC14L2 regulates the transport of cholesterol in non-small cell lung cancer through SCARB1.
Article in Lipids in health and disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Multi-Omics Integration: Predicting Progression and Optimizing Clinical Treatment of Hepatocellular Carcinoma Through Malignant-Cell-Related Genes.International journal of molecular sciences · 2025Article
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5 authors.
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Abstract
backgroundInhibiting cholesterol metabolism has shown great potential in non-small cell lung cancer (NSCLC). However, the regulatory mechanism of the lipid metabolism key factor Sect. 14-like lipid binding 2 (SEC14L2) in NSCLC remains unclear. This study investigates the effects of differentially expressed genes related to cholesterol metabolism on the development of NSCLC.
methodsCox regression and survival analysis were performed to screen cholesterol metabolism-related genes and predict survival prognosis in NSCLC patients. The proliferation and migration of NSCLC cells were assessed by CCK-8, EdU, colony formation and wound-healing assay. Cholesterol depletion and rescue trials were used to evaluate the effect of SEC14L2 on cholesterol transport in NSCLC cells. IF and Co-IP were used to analyze the targeting relationship between SEC14L2 and scavenger receptor class B member 1 (SCARB1).
resultsSEC14L2 was a key gene related to prognosis in NSCLC patients and was highly expressed in A549 and Calu-1 cells. Subsequent studies demonstrated that knockdown of SEC14L2 significantly reduced the proliferation and migration of NSCLC cells, resulting in inhibited tumor growth. Furthermore, both in vitro and in vivo experiments indicated that SEC14L2 regulated cholesterol uptake. Silencing SEC14L2 partially counteracted the promotion of cholesterol content by MβCD-chol in A549 and Calu-1 cells. We then verified that there was a protein interaction between SEC14L2 and SCARB1.
conclusionSEC14L2 promoted cholesterol uptake in NSCLC cells by up-regulating SCARB1 expression, thereby promoting NSCLC development.
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