ArticleFEBS open bio2021
Sulfasalazine synergistically enhances the inhibitory effects of imatinib against hepatocellular carcinoma (HCC) cells by targeting NFκB, BCR/ABL, and PI3K/AKT signaling pathway-related proteins.
Article in FEBS open bio, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- A Prognostic Model Based on Adipokine-Related Genes for Hepatocellular Carcinoma: Assessment of Patient Outcomes and Tumor Microenvironment Characterization.Digestive diseases and sciences · 2026Article
- Enhanced antitumor efficacy of sulfasalazine and mesalazine in colorectal cancer through modulatory action of Lacticaseibacillus rhamnosus GG.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- Synergistic Targeting of Hepatocellular Carcinoma via Novel Regorafenib Combinations with Diosmin, Sulfasalazine, or Rosuvastatin.Biochemical genetics · 2026Article
- Flavonoid-mediated modulation of ferroptosis: therapeutic potential in gastrointestinal cancers.Journal of advanced research · 2026Review
- Unlocking ferroptosis in prostate cancer - the road to novel therapies and imaging markers.Nature reviews. Urology · 2024Review
- Targeting and regulation of autophagy in hepatocellular carcinoma: revisiting the molecular interactions and mechanisms for new therapy approaches.Cell communication and signaling : CCS · 2023Review
- Effect of PLC-β1/CaM signaling pathway mediated by AT1R on the occurrence and development of hepatocellular carcinoma.Cancer cell international · 2021Article
- Knockdown of FBI-1 Inhibits the Warburg Effect and Enhances the Sensitivity of Hepatocellular Carcinoma Cells to Molecular Targeted AgentsFrontiers in oncology · 2021Article
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1 author at 1 institution in 1 country.
Funding
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Abstract
Hepatocellular carcinoma (HCC) is the third leading cause of cancer-related fatalities worldwide. Identification of second-line therapies for patients with progressive HCC is urgently required as the use of sorafenib and/or regorafenib remains unsatisfactory. Imatinib, a small-molecule kinase inhibitor, is used to treat certain types of cancer, and nuclear factor κB (NFκB) is a positive regulator of cancer cell expansion. The combined use of tyrosine kinase and NFκB inhibitors may have potential for treating HCC. The aim of this work was to assess the potential anticarcinogenic effects of imatinib and sulfasalazine alone or in combination on the human HCC cell lines HEPG2 and Huh-7. Both drugs were shown to affect the phosphoinositide 3-kinase/protein kinase B, phosphorylated signal transducer and activator of translation (p-STAT-3), breakpoint cluster region protein/Abelson proto-oncogene and NFκB pathways. At the transcriptional level, imatinib and sulfasalazine were found to synergistically down-regulate c-MET gene expression. When compared with the activities of either medication alone, combined use of imatinib and sulfasalazine enhanced inhibition of HCC cell proliferation and extended induction of apoptosis. In summary, the presented data suggest that sulfasalazine synergistically potentiates the antitumor effects of imatinib.
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