作者: Sunwoo Park , Whasun Lim , Fuller W Bazer , Gwonhwa Song
关键词: Cancer research 、 MAPK/ERK pathway 、 Annexin 、 PI3K/AKT/mTOR pathway 、 Signal transduction 、 Naringenin 、 Unfolded protein response 、 Apoptosis 、 Biology 、 Endoplasmic reticulum
摘要: Study question Does the flavonoid naringenin inhibit proliferation of human endometriosis cells? Summary answer Naringenin suppresses and increases apoptosis via depolarization mitochondrial membrane potential generation reactive oxygen species (ROS) in cells. What is known already For management endometriosis, hormonal therapy commonly used to decrease production estrogens by ovaries, but that has limitations including undesirable side effects with long-term therapies. To overcome these limitations, it important discover novel compounds which have no adverse effects, expression target molecules involved pathogenesis endometriosis. design size, duration Well-established cell lines (VK2/E6E7 End1/E6E7) were purchased from American Type Culture Collection. Effects on VK2/E6E7 End1/E6E7 cells assessed diverse assays a dose- time-dependent manner. Participants/materials, setting, methods viability, (Annexin V expression, propidium iodide staining, TUNEL invasion assays), mitochondria-mediated apoptosis, ROS endoplasmic reticulum (ER) stress proteins determined. Signal transduction pathways response determined western blot analyses. Main results role chance In present study, we demonstrated suppressed increased through inducing pro-apoptotic proteins, Bax Bak, both lines. addition, ROS, ER stress, activation eIF2α IRE1α, GADD153 GRP78 dose-dependent Furthermore, induction MAPK inactivation PI3K Limitations reasons for caution Lack vivo animal studies major limitation this research. Effectiveness induce requires further investigation. Wider implications findings Our suggest promising therapeutic compound treatment women. funding/competing interest(s) This work was supported grants Korea Health Technology R&D Project Industry Development Institute (KHIDI), funded Ministry & Welfare, Republic (No. HI15C0810 awarded G.S. HI17C0929 W.L.). The authors declare there are conflicts interest.