ArticleOncology letters2014
VX680 suppresses the growth of HepG2 cells and enhances the chemosensitivity to cisplatin.
Article in Oncology letters, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
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- The Co-Administration of Paclitaxel with Novel Pyridine and Benzofuran Derivatives that Inhibit Tubulin Polymerisation: A Promising Anticancer Strategy.Pharmaceutics · 2025Article
- Discovery of a novel Aurora B inhibitor GSK650394 with potent anticancer and anti-Journal of enzyme inhibition and medicinal chemistry · 2022Article
- Inhibition of Angiogenesis and Extracellular Matrix Remodeling: Synergistic Effect of Renin-Angiotensin System Inhibitors and Bevacizumab.Frontiers in oncology · 2022Article
- Inhibition of AURKA kinase activity suppresses collective invasion in a microfluidic cell culture platform.Scientific reports · 2017Article
- The Aurora kinase inhibitors in cancer research and therapy.Journal of cancer research and clinical oncology · 2016Review
- The p38 MAPK inhibitor BIRB796 enhances the antitumor effects of VX680 in cervical cancer.Cancer biology & therapy · 2016Article
- AURKA is a predictor of chemotherapy response and prognosis for patients with advanced oral squamous cell carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2015Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
VX680 is an Aurora A inhibitor. It has been reported to inhibit the growth of the HepG2 cell line in several studies. However, whether it enhances chemosensitivity to cisplatin remains unclear. In this study, the synergistic effect of VX680 and cisplatin on the proliferation of HepG2 cells was determined by MTT assay. The changes in cell apoptosis were detected by flow cytometry. Aurora A, Bcl-2 and p53 protein levels were analyzed by western blotting. This study demonstrated that VX680, cisplatin and a combination of the two inhibit the growth of HepG2 cells in a dose- and time-dependent manner. A synergistic effect was observed with the combined therapy. Moreover, the inhibitory effect of VX680 was positively correlated with the expression of Aurora A. The rate of apoptosis in the combined group was significantly higher compared with that of the VX680 and cisplatin groups. In addition, VX680 and cisplatin increased the expression of the p53 protein. Cisplatin reduced the expression of Bcl-2 protein, while VX680 did not. In the combined group, the expression of Bcl-2 and p53 changed significantly compared with the single drug group and control group. This study suggests that Aurora A may represent a valid target in hepatocellular carcinoma. We also demonstrated that the Aurora A inhibitor VX680 has a synergistic effect with cisplatin.
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