文献类型：期刊文献

英文题名：Heat shock protein B8 promotes proliferation and migration in lung adenocarcinoma A549 cells by maintaining mitochondrial function

作者：Yu, Ling-Ling[1,2];Wang, Yuan[3];Xiao, Zu-Ke[2];Chen, Sheng-Song[2,4,5]

第一作者：Yu, Ling-Ling

通信作者：Chen, SS[1];Chen, SS[2];Chen, SS[3]

机构：[1]Nanchang Univ, Dept Rehabil Med, Affiliated Hosp 2, 1 Minde Rd, Nanchang 330006, Jiangxi, Peoples R China;[2]Nanchang Univ, Dept Pulm & Crit Care Med, Jiangxi Prov Peoples Hosp, 92 Aiguo Rd, Nanchang 330006, Jiangxi, Peoples R China;[3]Gansu Univ Chinese Med, Dept Grad Sch, 35 Dingxi East Rd, Lanzhou 730000, Peoples R China;[4]China Japan Friendship Hosp, Dept Pulm & Crit Care Med, 2 East Yinghua Rd, Beijing 100029, Peoples R China;[5]Chinese Acad Med Sci, Grad Sch, Peking Union Med Coll, 9 Dong Dan San Tiao, Beijing 100730, Peoples R China

第一机构：Nanchang Univ, Dept Rehabil Med, Affiliated Hosp 2, 1 Minde Rd, Nanchang 330006, Jiangxi, Peoples R China

通信机构：[1]corresponding author), Nanchang Univ, Dept Pulm & Crit Care Med, Jiangxi Prov Peoples Hosp, 92 Aiguo Rd, Nanchang 330006, Jiangxi, Peoples R China;[2]corresponding author), China Japan Friendship Hosp, Dept Pulm & Crit Care Med, 2 East Yinghua Rd, Beijing 100029, Peoples R China;[3]corresponding author), Chinese Acad Med Sci, Grad Sch, Peking Union Med Coll, 9 Dong Dan San Tiao, Beijing 100730, Peoples R China.

年份：2021

卷号：476

期号：1

起止页码：187

外文期刊名：MOLECULAR AND CELLULAR BIOCHEMISTRY

收录：;Scopus(收录号：2-s2.0-85091045774);WOS:【SCI-EXPANDED(收录号:WOS:000569322400001)】；

基金：This work was supported by the Natural Science Foundation of Jiangxi Province (20202BABL216035, 20202BAB206042), the National Natural Science Foundation excellent youth cultivation project (20202ZDB01017), the Science and technology plan project of Jiangxi Administration of traditional Chinese Medicine, China (2019A067).

语种：英文

外文关键词：Heat shock protein B8; Lung adenocarcinoma; A549 cells; Proliferation; Migration; Mitochondrial function

摘要：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 pcDNA-HSPB8 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.