| Comparison of anticancer effects of HDAC inhibitors CG-745 and SAHA in non-small lung cancer cells |
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Hyo Jin Kim, Ph.D., Ui Ri An, M.D., Han Jee Yoon, M.D., Hyun Lim, M.D., Ki Eun Hwang, M.D., Ph.D., Young Suk Kim, Ph.D., Hak Ryul Kim, M.D., Ph.D. |
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Division of Pulmonary Medicine, Department of Internal Medicine, Wonkwang University School of Medicine, Iksan, Republic of Korea |
Correspondence:
Hak Ryul Kim, Tel: +82 63 859 2583, Fax: +82 63 855 2025 ,
Email: kshryj@wonkwang.ac.kr
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Received: 8 July 2024 • Revised: 17 November 2024 • Accepted: 10 February 2025 |
| Abstract |
Background
Histone deacetylase (HDAC) inhibition offers the potential for anti-cancer effects in a variety of cancers, since HDAC plays an important role in cancer development and progression. Thus, we demonstrated the therapeutic efficacy of the new HDAC inhibitor, CG-745, in comparison with existing HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA) in non-small lung cancer (NSCLC) cells.
Methods
The effect of CG-745 on apoptosis and reactive oxygen species (ROS) dependent mitochondrial dysfunction in human A549 and H460 cells was investigated by Annexin V assay, MitoSoX and Western blot. Also, to confirm HDAC expression, it was analyzed using real-time PCR. To confirm the inhibitory effect of EMT on CG-745 by TGF-β1, Western blot, scratch analysis, and matrigel invasion analysis were performed.
Results
Compared to SAHA, CG-745 inhibited cell viability and mRNA expression of HDACs such as HDAC1, HDAC2, HDAC3 and HDAC8. It also caused apoptosis, ROS and mitochondrial dysfunction in a concentration-dependent manner. CG-745 reversed EMT induced by TGF-β1 in A549 and H460 cells, and inhibited migration and invasion increased by TGF-β1. CG-745 has been shown to inhibit EMT and induce apoptosis in NSCLC cells.
Conclusion
It suggests that CG-745 could be a new treatment strategy for treatment of NSCLC. |
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