ArticleEndocrine2022
ACLY inhibitors induce apoptosis and potentiate cytotoxic effects of sorafenib in thyroid cancer cells.
Article in Endocrine, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- New insights into the ACLY-mediated metabolic and epigenetic interplay in macrophages.Journal of enzyme inhibition and medicinal chemistry · 2026Review
- Fatty acids metabolic reprogramming and tumor microenvironment in pancreatic cancer: targeting pathways.Clinical and experimental medicine · 2026Review
- mBiochemical genetics · 2026Article
- Research progress and therapeutic strategies in hepatocellular carcinoma metabolic reprogramming.Journal of advanced research · 2026Review
- Metabolic reprogramming in cancer: signaling pathways and therapeutic targets.Molecular cancer · 2026Review
- The Lipid Line of Defence: Monounsaturated Fatty Acids (MUFAs) in Cancer and Ferroptosis.Oxidative medicine and cellular longevity · 2026Review
- Exploring the significance of fatty acid metabolism reprogramming in the pathogenesis of cancer and anticancer therapy.Annals of medicine · 2025Review
- Exosome-mediated metabolic reprogramming: effects on thyroid cancer progression and tumor microenvironment remodeling.Molecular cancer · 2025Review
- Post-translational modifications in anaplastic thyroid carcinoma: biological mechanisms and therapeutic potential.Cancer cell international · 2025Review
- Dendritic cells: understanding ontogeny, subsets, functions, and their clinical applications.Molecular biomedicine · 2025Review
- Reprogramming of fatty acid metabolism in thyroid cancer: Potential targets and mechanisms.Chinese journal of cancer research = Chung-kuo yen cheng yen chiu · 2025Article
- Reprogramming of Thyroid Cancer Metabolism: from Mechanism to Therapeutic Strategy.Molecular cancer · 2025Review
- SLC25A1 and ACLY maintain cytosolic acetyl-CoA and regulate ferroptosis susceptibility via FSP1 acetylation.The EMBO journal · 2025Article
- Acetyl-CoA synthesis in the skin is a key determinant of systemic lipid homeostasis.Cell reports · 2025Article
- Article
- Role of ATP citrate lyase and its complementary partner on fatty acid synthesis in gastric cancer.Scientific reports · 2024Article
- The Role of Lipid Metabolism Disorders in the Development of Thyroid Cancer.International journal of molecular sciences · 2024Review
- ATP Citrate Lyase is a General Tumour Biomarker and Contributes to the Development of Cutaneous Squamous Cell Carcinoma.Acta dermato-venereologica · 2024Article
- The Tricarboxylic Acid Cycle Metabolites for Cancer: Friend or Enemy.Research (Washington, D.C.) · 2024Review
- Apoptotic Effect of Gallic Acid via Regulation of p-p38 and ER Stress in PANC-1 and MIA PaCa-2 Cells Pancreatic Cancer Cells.International journal of molecular sciences · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeATP-citrate lyase (ACLY) is a critical enzyme at the intersection of glucose and lipid metabolism. ACLY is often upregulated or activated in cancer cells to accelerate lipid synthesis and promote tumor progression. In this study, we aimed to explore the possibility of utilizing ACLY inhibition as a new strategy in the treatment of thyroid cancer.
methodsBioinformatics analysis of the public datasets was performed. Thyroid cancer cells were treated with two different ACLY inhibitors, SB-204990 and NDI-091143.
resultsBioinformatics analysis revealed that ACLY expression was increased in anaplastic thyroid cancer. In thyroid cancer cell lines FTC-133 and 8505C, ACLY inhibitors suppressed monolayer cell growth and clonogenic ability in a dose-dependent and time-dependent manner. Flow cytometry analysis showed that ACLY inhibitors increased the proportion of sub-G1 cells in the cell cycle and the number of annexin V-positive cells. Immunoblotting confirmed caspase-3 activation and PARP1 cleavage following treatment with ACLY inhibitors. Compromised cell viability could be partially rescued by co-treatment with the pan-caspase inhibitor Z-VAD-FMK. Additionally, we showed that ACLY inhibitors impeded three-dimensional growth and cell invasion in thyroid cancer cells. Isobolograms and combination index analysis indicated that ACLY inhibitors synergistically potentiated the cytotoxicity rendered by sorafenib.
conclusionsTargeting ACLY holds the potential for being a novel therapeutic strategy for thyroid cancer.
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