ArticlePharmaceutical research2019
Knockdown of Orphan Transporter SLC22A18 Impairs Lipid Metabolism and Increases Invasiveness of HepG2 Cells.
Article in Pharmaceutical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Analysis of SLC genes alternative splicing identifies the SLC7A6 RI isoform as a therapeutic target for colorectal cancer.Cancer science · 2025Article
- Hepatic drug-metabolizing enzymes and drug transporters in Wilson's disease patients with liver failure.Pharmacological reports : PR · 2021Article
- Melatonin inhibits lipid accumulation to repress prostate cancer progression by mediating the epigenetic modification of CES1.Clinical and translational medicine · 2021Article
- A Syndrome of Variable Allergy, Short Stature, and Fatty Liver.Frontiers in genetics · 2021Article
- Deorphaning a solute carrier 22 family member, SLC22A15, through functional genomic studies.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020Article
- The Roles of ImprintedCancers · 2020Article
- Modeling allele-specific expression at the gene and SNP levels simultaneously by a Bayesian logistic mixed regression model.BMC bioinformatics · 2019Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
purposeThe aim of this work is to investigate the roles of solute carrier family 22 member 18 (SLC22A18) in lipid metabolism and in establishing the tumor phenotype of HepG2 cells.
methodsSLC22A18-knockdown HepG2 cells were established by stable transfection with shRNA. Protein expression levels were measured by quantitative proteomics and Western blot analysis. Cell growth was examined by cell counting kit. Accumulation of triglyceride-rich lipid droplets was measured by Oil-Red O staining. Cell migration and invasion were examined by Transwell assays.
resultsSLC22A18-knockdown HepG2 cells accumulated triglyceride-rich lipid droplets and showed decreased expression levels of lysosomal/autophagic proteins, suggesting that lipid degradation is suppressed. Growth of HepG2 cells was decreased by SLC22A18 knockdown, but was restored by free fatty acid supplementation. In addition, SLC22A18 knockdown decreased the expression of insulin-like growth factor-binding protein 1 (IGFBP-1) and increased the invasion ability of HepG2 cells. Exogenous IGFBP-1 blocked the increase of invasion activity induced by SLC22A18 knockdown.
conclusionOur results suggest that suppression of SLC22A18 decreased the supply of intracellular free fatty acids from triglyceride-rich lipid droplets by impairing the lysosomal/autophagy degradation pathway and reduced the invasive activity of HepG2 cells by decreasing IGFBP-1 expression.
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Registered trials
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