ArticleActa pharmacologica Sinica2012
The important roles of RET, VEGFR2 and the RAF/MEK/ERK pathway in cancer treatment with sorafenib.
Article in Acta pharmacologica Sinica, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.
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Who cites it
27 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.
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- Computational identification of potential VEGFR2 inhibitors using integrated pharmacophore modeling, QSAR analysis, molecular docking, dynamics simulation, and virtual screening followed by in vitro bioassays.Journal of computer-aided molecular design · 2026Article
- Rapid Microfluidic Drug Sensitivity Testing Within 5 Days Using Minimal Clinical Tumor Samples.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Sorafenib nanomedicine in HCC: nano-bio interactions and combination therapies.Journal of nanobiotechnology · 2026Review
- MOF enhances the sensitivity and selectivity of sorafenib as an anticancer drug against hepatocellular carcinoma and colorectal cancer in vitro.Scientific reports · 2025Article
- New pyrano-pyridine conjugates as potential anticancer agents: design, synthesis and computational studies.Future medicinal chemistry · 2024Article
- The Emerging Role of Long Noncoding RNAs in Sorafenib Resistance Within Hepatocellular Carcinoma.Cancers · 2024Review
- Anti-proliferation evaluation of new derivatives of indole-6-carboxylate ester as receptor tyrosine kinase inhibitors.Future medicinal chemistry · 2024Article
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- Integration of scRNA and bulk RNA-sequence to construct the 5-gene molecular prognostic model based on the heterogeneity of thyroid carcinoma endothelial cell.Acta biochimica et biophysica Sinica · 2024Article
- Tyrosine kinase inhibitors in osteosarcoma: Adapting treatment strategiesa.Journal of bone oncology · 2023Review
- New proapoptotic chemotherapeutic agents based on the quinolone-3-carboxamide scaffold acting by VEGFR-2 inhibition.Scientific reports · 2023Article
- Receptor Tyrosine Kinase Inhibitors for the Treatment of Recurrent and Unresectable Bone Sarcomas.International journal of molecular sciences · 2022Review
- Identification of Novel Cyanopyridones and Pyrido[2,3-Pharmaceuticals (Basel, Switzerland) · 2022Article
- RET signaling pathway and RET inhibitors in human cancer.Frontiers in oncology · 2022Review
- DHA-enriched phosphatidylcholine suppressed angiogenesis by activating PPARγ and modulating the VEGFR2/Ras/ERK pathway in human umbilical vein endothelial cells.Food science and biotechnology · 2021Article
- Pursuing Precision: Receptor Tyrosine Kinase Inhibitors for Treatment of Pediatric Solid Tumors.Cancers · 2021Review
- Kinase gene fusions: roles and therapeutic value in progressive and refractory papillary thyroid cancer.Journal of cancer research and clinical oncology · 2021Review
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- Receptor Tyrosine Kinases in Osteosarcoma Treatment: Which Is the Key Target?Frontiers in oncology · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo elucidate the roles of receptor tyrosine kinases RET and VEGFR2 and the RAF/MEK/ERK signaling cascade in cancer treatment with sorafenib.
methodsThe cell lines A549, HeLa, and HepG2 were tested. The enzyme activity was examined under cell-free conditions using 384-well microplate assays. Cell proliferation was evaluated using the Invitrogen Alarmar Blue assay. Gene expression was analyzed using the Invitrogen SYBR Green expression assays with a sequence detection system. Protein expression analysis was performed using Western blotting.
resultsSorafenib potently suppressed the activities of cRAF, VEGFR2, and RET with IC(50) values of 20.9, 4 and 0.4 nmol/L, respectively. Sorafenib inhibited cRAF, VEGFR2, and RET via non-ATP-competitive, ATP-competitive and mixed-type modes, respectively. In contrast, sorafenib exerted only moderate cytotoxic effects on the proliferation of the 3 cell lines. The IC(50) values for inhibition of A549, HeLa, and HepG2 cells were 8572, 4163, and 8338 nmol/L, respectively. In the 3 cell lines, sorafenib suppressed the cell proliferation mainly by blocking the MEK/ERK downstream pathway at the posttranscriptional level, which in turn regulated related gene expression via a feed-back mechanism.
conclusionThis study provides novel evidence that protein kinases RET and VEGFR2 play crucial roles in cancer treatment with sorafenib.
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