Salvianolic Acid B Suppresses Non-Small-Cell Lung Cancer Metastasis through PKM2-Independent Metabolic Reprogramming

作者全名："Zhang, Hong; Tang, Jianming; Cao, Yu; Wang, Tianhu"

作者地址："[Zhang, Hong; Tang, Jianming; Cao, Yu; Wang, Tianhu] Chongqing Med Univ, Affiliated Hosp 3, Dept Thorac Surg, Chongqing 401120, Peoples R China"

通信作者："Wang, TH (通讯作者)，Chongqing Med Univ, Affiliated Hosp 3, Dept Thorac Surg, Chongqing 401120, Peoples R China."

来源：EVIDENCE-BASED COMPLEMENTARY AND ALTERNATIVE MEDICINE

ESI学科分类：CLINICAL MEDICINE

WOS号：WOS:000793405600001

JCR分区：Q3

影响因子：2.65

年份：2022

卷号：2022

期号：　

开始页：　

结束页：　

文献类型：Article

关键词：　

摘要："Objective. Salvianolic acid B (Sal B) has been demonstrated to be a potential chemoprevention agent for several cancers. Herein, we investigated the pharmacological function of Sal B on non-small-cell lung cancer (NSCLC) metastasis. Methods. Two NSCLC cell lines (NCI-H2030 and NCI-H1650) were disposed of by 200 mu M Sal B or 10 mu M PKM2 agonist TEPP-46. Wound healing and transwell experiments were implemented for analyzing migratory and invasive capacities. Epithelial-to-mesenchymal transition (EMT) markers beta-catenin and E-cadherin were measured via western blotting. Cellular bioenergetics were evaluated with glucose uptake, lactate production, enolase activity, cellular ATP levels, as well as seahorse-based oxygen consumption rate (OCR), extracellular acidification rate (ECAR) analysis. Metabolic reprogramming markers PKM2, LDHA, and GLUT1 were detected via western blotting and immunofluorescence. Results. The results showed that Sal B disposal weakened the migration and invasion of NCI-H2030 and NCI-H1650 cells and inactivated the EMT process according to downregulation of beta-catenin and upregulation of E-cadherin. Sal B-treated NSCLC cells displayed decreased glucose uptake, lactate production, enolase activity, cellular ATP levels, OCR, and ECAR, indicating a reduction in metabolic reprogramming. Additionally, Sal B downregulated the expression of PKM2, LDHA, and GLUT1. TEPP-46 may reverse the inhibitory effect of Sal B on metastasis as well as metabolic reprogramming. Conclusion. Our findings provide evidence that Sal B enables to weaken NSCLC metastasis through PKM2-independent metabolic reprogramming, which sheds light on the promising therapeutic usage of Sal B in treating NSCLC."

基金机构：　

基金资助正文：