Myricanol 5-fluorobenzyloxy ether regulation of survivin pathway inhibits human lung adenocarcinoma A549 cells growth in
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(2020) 20:269
BMC Complementary Medicine and Therapies
RESEARCH ARTICLE
Open Access
Myricanol 5-fluorobenzyloxy ether regulation of survivin pathway inhibits human lung adenocarcinoma A549 cells growth in vitro Guan-hai Dai1*, Xuan Chen1, Ze-ming Ren1, Chen-jie Dai2, Ye-ling Tong1 and Ke-qun Chai3*
Abstract Background: This study aimed to explore the growth inhibitory effect of myricanol 5-fluorobenzyloxy ether (5FEM) and its underlying mechanisms in human lung adenocarcinoma A549 cells in vitro. Methods: 5FEM was obtained by the chemical modification of myricanol with fluorobenzyloxy ether at the OH(5) position. The cytotoxicity, cell apoptosis, cell cycle, mitochondrial membrane potential (ΔΨm), scratch test, colony formation, and the expression levels of the key survivin pathway-related genes in A549 were evaluated. Results: 5FEM could significantly inhibit A549 cell growth; induce cell apoptosis; increase G0/G1 population; reduce ΔΨm; inhibit cell migration and colony formation; upregulate caspase-9, P21, and Bax expression levels; and downregulate PARP, survivin, and Bcl-2 expression level. Conclusion: These results enhanced our understanding of 5FEM and aid the discovery of novel myricanol derivatives as potential antitumor agents. Keywords: Myricanol 5-fluorobenzyloxy ether, Antitumor, Human lung adenocarcinoma A549, Survivin pathway, Cell growth inhibition, Mitochondrial membrane potential
Background Lung cancer is one of the most common malignant tumors and has the highest incidence and mortality. Its 5year relative survival rate is generally < 15% [1, 2]. Lung cancer is divided into non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC), with the former accounting for 85% of all patients. The occurrence and development of NSCLC are closely related to external factors, such as smoking, air pollution, and genetic factors. Despite the availability of chemotherapy regimens, the * Correspondence: [email protected]; [email protected] 1 Zhejiang Academy of Traditional Chinese Medicine, Institute of Basic Medicine, Hangzhou 310007, China 3 Oncology Department, Tongde Hospital of Zhejiang Province, Hangzhou 310012, China Full list of author information is available at the end of the article
mortality rate of NSCLC has not decreased [3]. Thus, the invasion and metastatic mechanisms in NSCLC should be understood to improve treatment individualization. Inhibitor of apoptosis protein (IAP) family regulates apoptosis. As a new member of the recently discovered IAP family, survivin plays an important role in cell apoptosis and cell cycle regulation [4]. In 1997, Ambrosini et al. [5] firstly isolated survivin from the human genome library using effect cell protease receptor 1 cDNA and found that it is still the strongest apoptotic inhibitor protein. The gene is located on human chromosome 17q25, has a full length of ~ 14.5 kb, contains four exons and three introns, and encodes a survivin protein with a molecular weight of 16.3 kD and contains 142 amino acids [6]. Survivin inhibits cell apoptosi
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