Inhibition of EGFR and AKT Activity by Licochalcone H Inhibits Proliferation and Induces Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells

Seung-On Lee; Mee-Hyun Lee; Ah-Won Kwak; Jin-Young Lee; Goo Yoon; Sang Hoon Joo; Yung Hyun Choi; Jin Woo Park; Jung-Hyun Shim

doi:10.20944/preprints202308.0641.v1

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preprints.org > medicine and pharmacology > pharmacology and toxicology > doi: 10.20944/preprints202308.0641.v1

Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Inhibition of EGFR and AKT Activity by Licochalcone H Inhibits Proliferation and Induces Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells

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Version 1 : Received: 8 August 2023 / Approved: 8 August 2023 / Online: 9 August 2023 (03:01:44 CEST)

How to cite: Lee, S.; Lee, M.; Kwak, A.; Lee, J.; Yoon, G.; Joo, S.H.; Choi, Y.H.; Park, J.W.; Shim, J. Inhibition of EGFR and AKT Activity by Licochalcone H Inhibits Proliferation and Induces Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells. Preprints 2023, 2023080641. https://doi.org/10.20944/preprints202308.0641.v1 Lee, S.; Lee, M.; Kwak, A.; Lee, J.; Yoon, G.; Joo, S.H.; Choi, Y.H.; Park, J.W.; Shim, J. Inhibition of EGFR and AKT Activity by Licochalcone H Inhibits Proliferation and Induces Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells. Preprints 2023, 2023080641. https://doi.org/10.20944/preprints202308.0641.v1

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MDPI and ACS Style

Lee, S.; Lee, M.; Kwak, A.; Lee, J.; Yoon, G.; Joo, S.H.; Choi, Y.H.; Park, J.W.; Shim, J. Inhibition of EGFR and AKT Activity by Licochalcone H Inhibits Proliferation and Induces Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells. Preprints 2023, 2023080641. https://doi.org/10.20944/preprints202308.0641.v1

APA Style

Lee, S., Lee, M., Kwak, A., Lee, J., Yoon, G., Joo, S.H., Choi, Y.H., Park, J.W., & Shim, J. (2023). Inhibition of EGFR and AKT Activity by Licochalcone H Inhibits Proliferation and Induces Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells. Preprints. https://doi.org/10.20944/preprints202308.0641.v1

Chicago/Turabian Style

Lee, S., Jin Woo Park and Jung-Hyun Shim. 2023 "Inhibition of EGFR and AKT Activity by Licochalcone H Inhibits Proliferation and Induces Apoptosis in Oxaliplatin-Sensitive and -Resistant Colorectal Cancer Cells" Preprints. https://doi.org/10.20944/preprints202308.0641.v1

Abstract

Licochalcone H (LCH), a regioisomer of licochalcone C derived from the root of Glycyrrhiza inflata. CRC treatment has always been challenged by the development of resistance. We investigated the antiproliferative activity of LCH in oxaliplatin (Ox)-sensitive and -resistant CRC cells. LCH significantly inhibited cell viability and colony growth in both Ox-sensitive and Ox-resistant CRC cells. We found that LCH decreased epidermal growth factor receptor (EGFR) and AKT kinase activities and related activating signaling proteins including phospho (p)-EGFR and pAKT. A computational docking model indicated that LCH may interact with EGFR, AKT1, and AKT2 at the ATP-binding sites. LCH induced ROS generation, as verified by N-acetyl-L-cysteine (NAC) treatment, and increased the expression of the ER stress markers. LCH treatment of CRC cells induced depolarization of MMP and increased. Multi-caspase activity was induced by LCH treatment and confirmed by Z-VAD-FMK treatment. LCH increased the number of subG1 cells and arrested the cell cycle at the G1 phase. LCH inhibits the growth of Ox-sensitive and Ox-resistant CRC cells by targeting EGFR and AKT, and inducing ROS generation and ER stress-mediated apoptosis. Therefore, LCH could be a potential therapeutic agent for improving not only Ox-sensitive but also Ox-resistant CRC treatment.

Keywords

licochalcone H (LCH); oxaliplatin; colorectal cancer; EGFR; AKT; apoptosis

Subject

Medicine and Pharmacology, Pharmacology and Toxicology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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