Licochalcone A induces endoplasmic reticulum stress‐mediated apoptosis of endometrial cancer cells via upregulation of GRP78 expression

Author:

Wu Min‐Hua1,Hsieh Yi‐Hsien23ORCID,Lin Chia‐Liang24,Ying Tsung‐Ho56,Hsia Shih‐Min7,Hsieh Shu‐Ching3,Lee Chien‐Hsing89,Lin Chu‐Liang2

Affiliation:

1. Laboratory Department, Chung‐Kang Branch Cheng‐Ching General Hospital Taichung Taiwan

2. Institute of Medicine Chung Shan Medical University Taichung Taiwan

3. Department of Medical Research Chung Shan Medical University Hospital Taichung Taiwan

4. Department of Biochemistry, School of Medicine Chung Shan Medical University Taichung Taiwan

5. Department of Obstetrics and Gynecology, School of Medicine, College of Medicine Chung Shan Medical University Taichung Taiwan

6. Department of Obstetrics and Gynecology Chung Shan Medical University Hospital Taichung Taiwan

7. School of Nutrition and Health Sciences, College of Nutrition Taipei Medical University Taipei Taiwan

8. Division of Pediatric Surgery, Department of Surgery Children's Hospital of China Medical University Taichung Taiwan

9. School of Chinese Medicine, College of Chinese Medicine China Medical University Taichung Taiwan

Abstract

AbstractLicochalcone A (LicA), a natural compound extracted from licorice root, has been shown to exert a variety of anticancer activities. Whether LicA has such effects on endometrial cancer (EMC) is unclear. This study aims to investigate the antitumor effects of LicA on EMC. Our results show that LicA significantly reduced the viability and induced apoptosis of EMC cells and EMC‐7 cells from EMC patients. LicA was also found to induce endoplasmic reticulum (ER) stress, leading to increased expression of ER‐related proteins (GRP78/PERK/IRE1α/CHOP) in EMC cell lines. Suppression of GRP78 expression in human EMC cells treated with LicA significantly attenuated the effects of LicA, resulting in reduced ER‐stress mediated cell apoptosis and decreased expression of ER‐ and apoptosis‐related proteins. Our findings demonstrate that LicA induces apoptosis in EMC cells through the GRP78‐mediated ER‐stress pathway, emphasizing the potential of LicA as an anticancer therapy for EMC.

Funder

China Medical University Hospital

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine

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