Hao Ji1,2, Juan Wang1,2, Binbin Lu1,2, Juan Li1,2, Jing Zhou1,2, Li Wang1,2, Shufen Xu1,2, Peng Peng1,2, Xuezhen Hu3,4, Keming Wang5,6. 1. Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China. 2. The Second Clinical Medical College of Nanjing Medical University, Nanjing, China. 3. Jiangsu Provincial Hospital of Traditional Chinese Medicine, Nanjing, China. Njhxzh@126.com. 4. Department of Radiology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, 210000, Jiangsu, People's Republic of China. Njhxzh@126.com. 5. Department of Oncology, Second Affiliated Hospital, Nanjing Medical University, Nanjing, 210000, Jiangsu, People's Republic of China. kemingwang@njmu.edu.cn. 6. The Second Clinical Medical College of Nanjing Medical University, Nanjing, China. kemingwang@njmu.edu.cn.
Abstract
BACKGROUND: LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration. METHODS: We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1. RESULTS: AGAP2-AS1 was significantly upregulated in CCA tumor tissues. SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA. CONCLUSIONS: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.
BACKGROUND: LncRNA can regulate gene at various levels such as apparent genetics, alternative splicing, and regulation of mRNA degradation. However, the molecular mechanism of LncRNA in cholangiocarcinoma is still unclear. This deserves further exploration. METHODS: We investigated the expression of AGAP2-AS1 in 32 CCA tissues and two CCA cell lines. We found a LncRNA AGAP2-AS1 which induced by SP1 has not been reported in CCA, and Knockdown and overexpression were used to investigate the biological role of AGAP2-AS1 in vitro. CHIP and RIP were performed to verify the putative targets of AGAP2-AS1. RESULTS:AGAP2-AS1 was significantly upregulated in CCA tumor tissues. SP1 induced AGAP2-AS1 plays an important role in tumorigenesis. AGAP2-AS1 knockdown significantly inhibited proliferation and caused apoptosis in CCA cells. In addition, we demonstrated that AGAP2-AS1 promotes the proliferation of CCA. CONCLUSIONS: We conclude that the long non-coding RNA AGAP2-AS1 plays a role in promoting the proliferation of cholangiocarcinoma.