ArticleMolecular biology reports2020
Dysregulated lipid metabolism in hepatocellular carcinoma cancer stem cells.
Article in Molecular biology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 42 citations in OpenAlex.
- Non-small cell lung cancer and metabolism research from 2013 to 2023: a visual analysis and bibliometric study.Frontiers in oncology · 2024Pooled it
- Reprogramming Metabolism and Immunity: Nanotechnology's Promise for Hepatocellular Carcinoma Precision Therapy.International journal of nanomedicine · 2026Review
- Lipid metabolism in cancer cells: Its role in hepatocellular carcinoma progression and therapeutic resistance.Hepatology communications · 2025Review
- Identification of New CD36 Antagonists by Structure-Based Virtual Screening.Chemical biology & drug design · 2025Article
- Cancer stem cells: landscape, challenges and emerging therapeutic innovations.Signal transduction and targeted therapy · 2025Review
- Review
- Cancer stem cells in personalized therapy: mechanisms, microenvironment crosstalk, and therapeutic vulnerabilities.Frontiers in cell and developmental biology · 2025Review
- Discovery andFrontiers in immunology · 2025Article
- Research advances in traditional Chinese medicine formulae and active components targeting lipid metabolism for hepatocellular carcinoma therapy.Frontiers in pharmacology · 2025Review
- CDT1 is a Potential Therapeutic Target for the Progression of NAFLD to HCC and the Exacerbation of Cancer.Current genomics · 2025Article
- Assessing CD36 and CD47 expression levels in solid tumor indications to stratify patients for VT1021 treatment.NPJ precision oncology · 2024Article
- Role of ATP citrate lyase and its complementary partner on fatty acid synthesis in gastric cancer.Scientific reports · 2024Article
- Metabolic Crossroad Between Macrophages and Cancer Cells: Overview of Hepatocellular Carcinoma.Biomedicines · 2024Review
- Targeting Lipid Metabolism in Cancer Stem Cells for Anticancer Treatment.International journal of molecular sciences · 2024Review
- Multidimensional analysis of tumor stem cells: from biological properties, metabolic adaptations to immune escape mechanisms.Frontiers in cell and developmental biology · 2024Review
- Advances in Targeted Drug Resistance Associated with Dysregulation of Lipid Metabolism in Hepatocellular Carcinoma.Journal of hepatocellular carcinoma · 2024Review
- GPAT3 is a potential therapeutic target to overcome sorafenib resistance in hepatocellular carcinoma.Theranostics · 2024Article
- Lipid metabolism dynamics in cancer stem cells: potential targets for cancers.Frontiers in pharmacology · 2024Review
- Metabolic Profiles of Cancer Stem Cells and Normal Stem Cells and Their Therapeutic Significance.Cells · 2023Review
- Identification of a gene set that maintains tumorigenicity of the hepatocellular carcinoma cell line Li-7.Human cell · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
According to the stem cell theory for cancer, hepatocellular carcinomas are sustained by a group of cancer stem cells (CSCs) which are responsible for resistance to chemotherapy. In the present study we aimed to examine lipid metabolism in cancer stem cells induced by long-term treatment with sorafenib and its relationship with acquisition of a CSC-like phenotype. Two cell lines (HepG2SF1 and Huh7SF1) were generated by incubation with a step-wise increase of sorafenib concentrations for 10 months. These cell lines displayed stem-like characteristics like increase in the expression of ABCB1A, Nanog and Oct4 as well as an E-cadherin/N-cadherin switch. HepG2SF1 and Huh7SF1 cells showed intracellular accumulation of neutral lipids, assessed by flow cytometry and confocal microscopy. The exam of lipid metabolism revealed that HepG2SF1 and Huh7SF1 cells increased the expression of the enzymes involved in de novo lipid synthesis ATP-citrate lyase (ACLY), acetyl-CoA carboxylase (ACC) and fatty acid synthase (FASN) and that of the fatty acid transporter CD36. In addition, these CSC-like cells had enhanced expression of the lipogenic transcription factor SREBP1c. Analysis of the key metabolic sensor AMP-activated kinase (AMPK) demonstrated that both AMPK phosphorylation and levels were decreased in the CSC-like cells compared to their parental cells. Interestingly, transfection of HepG2SF1 and Huh7SF1 cells with AMPK, restored the levels of the lipogenic enzymes and SREBP1c and decreased the intracellular lipid accumulation. Furthermore, AMPK transfection decreased the stemness markers and inhibited the E-cadherin/N-cadherin switch. Targeting AMPK and lipid metabolism of hepatocellular cancer stem cells is a promising strategy to face stemness and chemotherapy resistance.
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