LncRNA-SRA1 Suppresses Osteosarcoma Cell Proliferation While Promoting Cell Apoptosis

• Published in: Technology in cancer research & treatment 2019, Vol.18, p.1533033819841438-1533033819841438
• Main Authors: Guo, Wen, Jiang, Haitao, Li, Haijun, Li, Fang, Yu, Qing, Liu, Yu, Jiang, Weiwei, Zhang, Ming
• Format: Article
• Language: English
• Subjects: Adolescents; Apoptosis; Apoptosis - genetics; Bone cancer; Bone Neoplasms - genetics; Bone tumors; Carrier Proteins - genetics; Cell adhesion & migration; Cell death; Cell growth; Cell Line, Tumor; Cell migration; Cell Movement - genetics; Cell Proliferation; Computational Biology - methods; Flow cytometry; Gene Expression Profiling; Gene Expression Regulation, Neoplastic; Humans; MicroRNAs; MicroRNAs - genetics; miRNA; Original; Osteosarcoma; Osteosarcoma - genetics; Osteosarcoma cells; Polymerase chain reaction; RNA Interference; RNA, Long Noncoding - genetics; RNA-mediated interference; Sarcoma; Therapeutic applications; Wound healing
• ISSN: 1533-0346; 1533-0338
• DOI: 10.1177/1533033819841438

Objective: Osteosarcoma is a common malignant bone tumor that is frequently found in the long bones of children and adolescents. The aim of this study is to examine long noncoding RNA-steroid receptor RNA activator 1 expression in osteosarcoma to explore the biological function of long noncoding RNA steroid receptor RNA activator 1 on proliferation, migration, and invasion along with apoptosis and its regulatory mechanism, which would facilitate the early diagnosis and targeted therapy of osteosarcoma. Methods: First, microarray analysis was applied to determine the expression of long noncoding RNAs in osteosarcoma tissues and paired normal tissues. Then, quantitative real-time polymerase chain reaction was utilized to validate microarray findings. Next, osteosarcoma cancerous cell lines SJSA-1 and U2OS were transfected with pcDNA3.1-SRA1 or pCMV-sh-SRA1 to increase or decrease steroid receptor RNA activator 1 expression levels, and microRNA-208a inhibitors, mimic to investigate the effects of microRNA-208a on osteosarcoma as well as the regulatory relation between long noncoding RNA steroid receptor RNA activator 1 and microRNA-208a. Cell proliferation was evaluated through Cell Counting Kit-8 and colony formation assays. Flow cytometry analysis was conducted to evaluate the apoptosis ratio. The migration and invasion abilities were measured using wound-healing and transwell assays. Results: Long noncoding RNA-steroid receptor RNA activator 1 expression was downregulated in osteosarcoma tissues and cells compared with that in corresponding normal tissues, whereas microRNA-208a expression was upregulated in osteosarcoma tissues. Moreover, the restoration of long noncoding RNA steroid receptor RNA activator 1 inhibited cell proliferation, and upregulation of long noncoding RNA steroid receptor RNA activator 1 restrained cell migration and invasion but boosted the apoptosis rate in osteosarcoma cells. In addition, long noncoding RNA steroid receptor RNA activator 1 targeting microRNA-208a was involved in the progression of osteosarcoma. Furthermore, upregulating microRNA-208a exerted similar roles of silencing long noncoding RNA steroid receptor RNA activator 1 in cell apoptosis, proliferation, migration, and invasion, which were reversed by enhancing the expression of long noncoding RNA steroid receptor RNA activator 1. Conclusions: In our study, long noncoding RNA steroid receptor RNA activator 1 played an antitumor role in osteosarcoma as it reduced cell