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Beta-naphthoflavone and doxorubicin synergistically enhance apoptosis in human lung cancer cells by inducing doxorubicin accumulation, mitochondrial ROS generation, and JNK pathway signaling

Hoang Department of Biochemistry and Molecular Biology, Graduate School, College of Medicine, Kyung Hee University, Seoul, 130-701, South Korea|
Joohun (7202103373) | Sung Soo (57196227865); Ha | Insug (7203062725); Kim | Wonchae (12243040400); Kang | Quynh Hoa (57195243697); Choe | Lochana Mangesh (57355861400); Tran | Minhyeok (57215383011); Kovale Department of Biology and Environment, Ho Chi Minh City University of Food Industry, Ho Chi Minh, Viet Nam| Dang Hieu (57219174803); Song Applied DNA Technology Laboratory, Institute of Biotechnology, Vietnam Academy of Sciences and Technology, Viet Nam|

Biochemical and Biophysical Research Communications Số , năm 2022 (Tập 635, trang 37-45)

ISSN: 0006291X

ISSN: 0006291X

DOI: 10.1016/j.bbrc.2022.10.015

Tài liệu thuộc danh mục:



Từ khóa: Antineoplastic Agents; Apoptosis; beta-Naphthoflavone; Cell Line, Tumor; Doxorubicin; Female; Humans; Lung Neoplasms; MAP Kinase Signaling System; Reactive Oxygen Species; antineoplastic agent; beta naphthoflavone; doxorubicin; reactive oxygen metabolite; apoptosis; female; human; lung tumor; MAPK signaling; metabolism; tumor cell line
Tóm tắt tiếng anh
Doxorubicin is one of the most effective chemotherapeutic agents available for treating various cancers, including lung cancer—the leading cause of cancer death in both men and women. However, its clinical application has been impeded by severe adverse effects, notably cardiotoxicity. Development of cellular resistance to doxorubicin is another major obstacle that must be overcome for broader application of the drug. In the present study, we examined the therapeutic potential of beta-naphthoflavone (BNF), a synthetic derivative of a naturally occurring flavonoid, in combination with doxorubicin for the treatment of lung cancer. Among our novel observations were that BNF enhances the efficacy of doxorubicin by inducing doxorubicin accumulation, mitochondrial ROS generation, and JNK pathway signaling in lung cancer cells. These combined effects were also evident in many other cancer cell types. BNF further exhibited synergistic induction of apoptosis in lung cancer cells when combined with several other cancer drugs, including irinotecan, cisplatin, and 5-fluorouracil. Our results suggest that BNF can be developed as a promising adjuvant agent for enhancing the efficacy of doxorubicin. © 2022

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