Biomol Ther.
2022 Jan;30(1):72-79. 10.4062/biomolther.2021.149.
Licochalcone H Induces Cell Cycle Arrest and Apoptosis in Human Skin Cancer Cells by Modulating JAK2/STAT3 Signaling
- Affiliations
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- 1Department of Dental Pharmacology, School of Dentistry, Jeonbuk National University, Jeonju 54896, Republic of Korea
- 2College of Pharmacy, Daegu Catholic University, Gyeongsan 38430, Republic of Korea
- 3Department of Pharmacy, College of Pharmacy, Mokpo National University, Muan 58554, Republic of Korea
- 4Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon 34141, Republic of Korea
- 5College of Korean Medicine, Dongshin University, Naju 58245, Republic of Korea
- 6Biosystem Research Group, Department of Predictive Toxicology, Korea Institute of Toxicology, Daejeon 34114, Republic of Korea
- 7The China –US (Henan) Hormel Cancer Institute, Zhengzhou, Henan 450008, China
- KMID: 2524149
- DOI: http://doi.org/10.4062/biomolther.2021.149
Abstract
- Licochalcone H (LCH) is a phenolic compound synthetically derived from licochalcone C (LCC) that exerts anticancer activity. In this study, we investigated the anticancer activity of LCH in human skin cancer A375 and A431 cells. The 3-(4,5-dimethylthiazol-2-yl)-5-(3-carboxymethoxyphenyl)-2-(4-sulfophenyl)-2H-tetrazolium (MTS) cell viability assay was used to evaluate the antiproliferative activity of LCH. Cell cycle distribution and the induction of apoptosis were analyzed by flow cytometry. Western blotting assays were performed to detect the levels of proteins involved in cell cycle progression, apoptosis, and the JAK2/STAT3 signaling pathway. LCH inhibited the growth of cells in dose- and time-dependent manners. The annexin V/propidium iodide double staining assay revealed that LCH induced apoptosis, and the LCH-induced apoptosis was accompanied by cell cycle arrest in the G1 phase. Western blot analysis showed that the phosphorylation of JAK2 and STAT3 was decreased by treatment with LCH. The inhibition of the JAK2/STAT3 signaling pathway by pharmacological inhibitors against JAK2/STAT3 (cryptotanshinone (CTS) and S3I-201) simulated the antiproliferative effect of LCH suggesting that LCH induced apoptosis by modulating JAK2/STAT3 signaling.
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