Heat shock protein B8 promotes proliferation and migration in lung adenocarcinoma A549 cells by maintaining mitochondria
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Heat shock protein B8 promotes proliferation and migration in lung adenocarcinoma A549 cells by maintaining mitochondrial function Ling‑Ling Yu1,2 · Yuan Wang3 · Zu‑Ke Xiao2 · Sheng‑Song Chen2,4,5 Received: 6 April 2020 / Accepted: 2 September 2020 © Springer Science+Business Media, LLC, part of Springer Nature 2020
Abstract Heat shock protein B8 (HSPB8) impacts on tumor proliferation and migration of malignancy. However, the role of HSPB8 in lung adenocarcinoma (LUAC) remains unclear. The aim of this study, therefore, was to clarify whether HSPB8 could bring benefits to proliferation and migration of LUAC and its underlying mechanisms. The expression of HSPB8 was first evaluated by immunohistochemistry in 35 LUAC samples. Then, A549 lung adenocarcinoma cells were transfected with pcDNAHSPB8 or si-HSPB8 to induce HSPB8 overexpression and silence. Cellular activity was evaluated with a Cell Counting Kit-8 (CCK-8) assay. Cell proliferation and migration were observed by EdU assay and scratch assay. Mitochondria-specific reactive oxygen species (mtROS) and membrane potential were measured using MitoSOX Red probe and JC-1 staining. Superoxide dismutase (SOD) activities and malondialdehyde (MDA) level were measured using commercial kits, respectively. HSPB8 protein, mitochondrial fusion protein MFN2 and mitochondrial fission protein p-Drp1/Drp1 were measured using western blot. Compared with the normal tissues, the expression of HSPB8 protein was higher in LUAC tissues and upregulation of HSPB8 protein was related to tumor size and tumor location. Furthermore, HSPB8 overexpression aggravated cell proliferation and migration of A549 cells. Mechanistically, HSPB8 suppressed mitochondrial impairment, leading to promoting the progress of A549 lung adenocarcinoma cells. These data demonstrate that HSPB8 plays an important role in progression of LUAC and may be a new target to treat LUAC. Keywords Heat shock protein B8 · Lung adenocarcinoma · A549 cells · Proliferation · Migration · Mitochondrial function
* Sheng‑Song Chen [email protected] 1
Department of Rehabilitation Medicine, The Second Affiliated Hospital of Nanchang University, No. 1 Minde Road, Nanchang 330006, Jiangxi, People’s Republic of China
2
Department of Pulmonary and Critical Care Medicine, Jiangxi Provincial People’s Hospital Affiliated to Nanchang University, No. 92 Aiguo Road, Nanchang 330006, Jiangxi, People’s Republic of China
3
Department of Graduate School, Gansu University of Chinese Medicine, No. 35 Dingxi East Road, Chengguan District 730000, Lanzhou, People’s Republic of China
4
Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, No 2, East Yinghua Road, Chaoyang District 100029, Beijing, People’s Republic of China
5
Graduate School of Peking Union Medical College, Chinese Academy of Medical Sciences, No 9, Dong Dan San Tiao, Dongcheng District 100730, Beijing, People’s Republic of China
Introduction Lung cancer is the most commonly malignancy and the leading cause of death among all type
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