ArticleCancer management and research2021
Apatinib Promotes Ferroptosis in Colorectal Cancer Cells by Targeting ELOVL6/ACSL4 Signaling.
Article in Cancer management and research, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Ferroptosis and ferritinophagy in diabetes complications.Molecular metabolism · 2022Pooled it
- Review
- Targeting cell death: a promising approach for colorectal cancer therapy.Cancer cell international · 2026Review
- Apatinib and silver nanoparticles synergize against gastric cancer through the PI3K/Akt signaling pathway-mediated ferroptosis.Journal of pharmaceutical analysis · 2026Article
- Elovl6 inhibits colorectal cancer progression through stearic acid-mediated mitochondrial fusion and metabolic reprogramming.Science advances · 2026Article
- Ferroptosis as a therapeutic target in glioblastoma: Mechanisms and emerging strategies.Molecular therapy. Nucleic acids · 2025Review
- Development of a bispecific CDH17-GUCY2C ADC bearing the ferroptosis inducer RSL3 for the treatment of colorectal cancer.Cell death discovery · 2025Article
- CircRNA_1156 Attenuates Neodymium Nitrate-Induced Hepatocyte Ferroptosis by Inhibiting the ACSL4/PKCβII Signaling Pathway.Antioxidants (Basel, Switzerland) · 2025Article
- Apatinib Mesylate Inhibits Cell Proliferation and the Metastasis of Esophageal Squamous Cell Carcinoma Through ERK/ELK-1/Snail Pathway.Cell biochemistry and biophysics · 2025Article
- A comprehensive bioinformatics analysis of fatty acid metabolism-associated genes in the diagnosis and prognosis of head and neck squamous cell carcinoma.Research in pharmaceutical sciences · 2025Article
- Male-specific lethal 1 (MSL1) promotes Erastin-induced ferroptosis in colon cancer cells by regulating the KCTD12-SLC7A11 axis.Cell death & disease · 2025Article
- Analysis of expression characteristics of ferroptosis-related lncRNAs in gastrointestinal cancer patients in Asia.Discover oncology · 2025Article
- The prognostic importance of the negative regulators of ferroptosis, GPX4 and HSPB1, in patients with colorectal cancer.Oncology letters · 2025Article
- Application prospects of ferroptosis in colorectal cancer.Cancer cell international · 2025Review
- Dissecting the opposing regulatory functions of endogenous nitric oxide production in colorectal cancer initiation, adaptive immune response alterations, and ferroptosis execution.Oncology reviews · 2025Review
- Harnessing the gut microbiome to modulate ferroptosis: a metabolic strategy for the treatment of digestive tract cancers.Frontiers in immunology · 2025Review
- Research progress on ferroptosis and PARP inhibitors in ovarian cancer: action mechanisms and resistance mechanisms.Frontiers in pharmacology · 2025Review
- Predictive and prognostic value of ACSL4 and GPX4 in patients with esophageal squamous cell carcinoma receiving post-operative radiotherapy.Journal of thoracic disease · 2024Article
- Therapeutic efficacy of ferroptosis in the treatment of colorectal cancer (Review).Oncology letters · 2024Review
- Inhibition of FSP1: A new strategy for the treatment of tumors (Review).Oncology reports · 2024Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundColorectal cancer (CRC) is a common digestive system malignancy. Ferroptosis, a new form of regulated cell death, plays a vital role in the pathogenesis and therapy of cancers.
objectiveWe aimed to study the role of apatinib in ferroptosis of CRC cells and its potential mechanisms. MATERIALS AND
methodsHuman CRC HCT116 cells were exposed to apatinib. Cell viability was examined using a CCK-8 kit. The concentrations of intracellular iron and reactive oxygen species (ROS) were detected using kits. Additionally, Western blot analysis was used to determine the expression of ferroptosis-related proteins. Elongation of very long-chain fatty acids family member 6 (ELOVL6) was one of the targets of apatinib predicted by SwissTargetPrediction. Therefore, ELOVL6 expression was evaluated after treatment with apatinib. Subsequently, the effects of ELOVL6 overexpression on ferroptosis of HCT116 cells were investigated. Finally, STRING database was applied to predict the potential proteins interacting with ELOVL6, and co-immunoprecipitation (co-IP) assay was applied for confirmation.
resultsResults indicated that apatinib decreased cell viability and increased the contents of intracellular iron ROS. Moreover, significantly upregulated ACSL4 expression was observed, accompanied by notable downregulation of GPx4 and FTH1 expression after apatinib exposure. Furthermore, ELOVL6 expression was remarkably enhanced in HCT116 cells, which was dramatically inhibited under apatinib intervention. ELOVL6 overexpression reversed the effects of apatinib on cell viability and ferroptosis of HCT116 cells. Moreover, ACSL4, a vital regulator of ferroptosis, could interact with ELOVL6 directly, which was confirmed by the result of co-IP.
conclusionThese findings demonstrated that apatinib promoted ferroptosis in CRC cells by targeting ELOVL6/ACSL4, providing a new mechanism support for apatinib application in the clinical treatment of CRC.
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