C-C Hu1, Y-W Liang, J-L Hu, L-F Liu, J-W Liang, R Wang. 1. Department of Oncology, the Affiliate Hospital of Chengde Medical University, Chengde, China. chanchanhu@126.com.
Abstract
OBJECTIVE: To clarify the potential function of long non-coding RNA (lncRNA) RUSC1-AS1 in regulating the progression of breast cancer (BCa) and the underlying mechanism. PATIENTS AND METHODS: RUSC1-AS1 level in BCa tissues and adjacent normal tissues was first determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between RUSC1-AS1 expression with tumor size, clinical stage and overall survival of BCa patients was analyzed. Influences of RUSC1-AS1 knockdown on viability, clonality, cell cycle and apoptosis of BCa cell lines MCF-7 and BT549 were evaluated. Target genes of RUSC1-AS1 were predicted by bioinformatics, and their interaction was further confirmed by RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP) and rescue experiments. RESULTS: A higher abundance of RUSC1-AS1 was identified in BCa tissues relative to controls. The expression level of RUSC1-AS1 was positively correlated to tumor size and clinical grade, but negatively correlated to the overall survival of BCa patients. The silence of RUSC1-AS1 markedly inhibited viability, clonality, cell cycle progression, and induced apoptosis of MCF-7 and BT549 cells. Finally, CDKN1A and KLF2 were found to be the target genes of RUSC1-AS1, which were tumor-suppressor genes involved in RUSC1-AS1-mediated BCa progression. CONCLUSIONS: RUSC1-AS1 is highly expressed in BCa, which promotes the progression of BCa through mediating CDKN1A and KLF2. RUSC1-AS1 may serve as a potential hallmark for BCa.
OBJECTIVE: To clarify the potential function of long non-coding RNA (lncRNA) RUSC1-AS1 in regulating the progression of breast cancer (BCa) and the underlying mechanism. PATIENTS AND METHODS: RUSC1-AS1 level in BCa tissues and adjacent normal tissues was first determined by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). The correlation between RUSC1-AS1 expression with tumor size, clinical stage and overall survival of BCa patients was analyzed. Influences of RUSC1-AS1 knockdown on viability, clonality, cell cycle and apoptosis of BCa cell lines MCF-7 and BT549 were evaluated. Target genes of RUSC1-AS1 were predicted by bioinformatics, and their interaction was further confirmed by RNA immunoprecipitation (RIP), chromatin immunoprecipitation (ChIP) and rescue experiments. RESULTS: A higher abundance of RUSC1-AS1 was identified in BCa tissues relative to controls. The expression level of RUSC1-AS1 was positively correlated to tumor size and clinical grade, but negatively correlated to the overall survival of BCa patients. The silence of RUSC1-AS1 markedly inhibited viability, clonality, cell cycle progression, and induced apoptosis of MCF-7 and BT549 cells. Finally, CDKN1A and KLF2 were found to be the target genes of RUSC1-AS1, which were tumor-suppressor genes involved in RUSC1-AS1-mediated BCa progression. CONCLUSIONS:RUSC1-AS1 is highly expressed in BCa, which promotes the progression of BCa through mediating CDKN1A and KLF2. RUSC1-AS1 may serve as a potential hallmark for BCa.