Hemistepsin A induces apoptosis by modulating the reactive oxygen species-dependent PI3K/Akt signaling pathway in human lung carcinoma A549 cells

• 발행기관: 대한생리학회-대한약리학회
• 저자명: So Young Kim Gi-Young Kim Yung Hyun Choi
• 간행물 정보: 『The Korean Journal of Physiology & Pharmacology』제29권 제5호, 625~636쪽, 전체 12쪽
• 주제분류: 의약학 > 의학일반
• 파일형태: PDF
• 발행일자: 2025.09.01

국문 초록

Hemistepsin A is a sesquiterpene lactone isolated from plants of the family. Recently, this compound was reported to be a bioactive compound that is beneficial for numerous health problems without side effects; however, its effect on lung cancer cells has not yet been studied. Therefore, in this study, we investigated the anticancer activity of hemistepsin A in human lung carcinoma A549 cells. This study showed that treatment with hemistepsin A induces apoptosis by activating caspase cascade and reducing the expression of inhibitors of apoptotic protein family members. Additionally, hemistepsin A disrupted mitochondrial integration by altering the levels of Bcl-2 family proteins to increase the cytoplasmic release of cytochrome c. Moreover, hemistepsin A reduced the activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway, and pretreatment with a PI3K inhibitor markedly augmented the cytotoxic effect of hemistepsin A on A549 cells. Furthermore, hemistepsin A significantly enhanced the production of intracellular and mitochondrial reactive oxygen species (ROS), whereas ROS scavengers restored the reduced viability by attenuating DNA damage and apoptosis by blocking the hemistepsin A-mediated inactivation of the PI3K/Akt pathway. Our findings demonstrate that hemistepsin A induces apoptosis in A549 cells by generating ROS, which subsequently inhibits the PI3K/Akt pathway, suggesting that ROS generation is involved as an early inducer of hemistepsin A-mediated anticancer activity.

목차

INTRODUCTION

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DISCUSSION

REFERENCES

키워드

A549 cells Apoptosis Lactones, Phosphatidylinositol 3-kinase Reactive oxygen species