Zhou Dong1, Yun Wang2. 1. Department of Orthopaedic Spine, Hefei Binhu Hospital, Hefei, Anhui Province, 230000, China. Electronic address: DongZhou06@163.com. 2. Department of Electrocardiology, The Second Hospital of Anhui Medical University, Hefei, Anhui Province, 230000, China. Electronic address: stmosaic@vip.qq.com.
Abstract
BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported in human cancers as regulators for biological processes. LncRNA bladder cancer associated transcript 1 (BLACAT1) has been found to exert oncogenic function in cervical cancer and lung cancer. However, whether it can regulate the biological processes in osteosarcoma (OS) is still unclear. This study aims to examine the potential effect of dysregulated BLACAT1 on the progression of OS. METHODS: The expression pattern of BLACAT1 in OS tissues and cell lines was detected by qRT-PCR assay. Gain or loss-of function assays were designed and conducted to determine the effect of BLACAT1 overexpression or knockdown on the OS cell proliferation, apoptosis, invasion and migration. RNA pull-down assay and western blot analysis were performed to identify the relationship between BLACAT1 and signal transducer and activator of transcription 3 (STAT3). RESULTS: BLACAT1 was upregulated in OS tissues and cells. Upregulation of BLACAT1 predicted unfavorable prognosis for patients with OS. Downregulation of BLACAT1 inhibited cell proliferation and invasion, whereas upregulation of BLACAT1 accelerated cell proliferation and invasion. More importantly, BLACAT1 could interact with STAT3 and regulat the phosphorylation of STAT3. CONCLUSIONS: LncRNA BLACAT1 contributes to the proliferation and migration of OS cells by regulating STAT3.
BACKGROUND: Long non-coding RNAs (lncRNAs) have been reported in humancancers as regulators for biological processes. LncRNA bladder cancer associated transcript 1 (BLACAT1) has been found to exert oncogenic function in cervical cancer and lung cancer. However, whether it can regulate the biological processes in osteosarcoma (OS) is still unclear. This study aims to examine the potential effect of dysregulated BLACAT1 on the progression of OS. METHODS: The expression pattern of BLACAT1 in OS tissues and cell lines was detected by qRT-PCR assay. Gain or loss-of function assays were designed and conducted to determine the effect of BLACAT1 overexpression or knockdown on the OS cell proliferation, apoptosis, invasion and migration. RNA pull-down assay and western blot analysis were performed to identify the relationship between BLACAT1 and signal transducer and activator of transcription 3 (STAT3). RESULTS:BLACAT1 was upregulated in OS tissues and cells. Upregulation of BLACAT1 predicted unfavorable prognosis for patients with OS. Downregulation of BLACAT1 inhibited cell proliferation and invasion, whereas upregulation of BLACAT1 accelerated cell proliferation and invasion. More importantly, BLACAT1 could interact with STAT3 and regulat the phosphorylation of STAT3. CONCLUSIONS: LncRNA BLACAT1 contributes to the proliferation and migration of OS cells by regulating STAT3.