Meile Mo1, Shun Liu1, Xiaoyun Ma1, Chao Tan1,2, Liangjia Wei1, Yonghong Sheng1, Yanye Song1, Xiaoyun Zeng1, Dongping Huang3, Xiaoqiang Qiu4. 1. Department of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China. 2. Department of Epidemiology and Statistics, School of Public Health, Guilin Medical University, Guilin, 541004, Guangxi, People's Republic of China. 3. Department of Sanitary Chemistry, School of Public Health, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China. 4. Department of Epidemiology, School of Public Health, Guangxi Medical University, Nanning, 530021, Guangxi, People's Republic of China. xqqiu9999@sina.com.
Abstract
BACKGROUND: Increasing evidence has shown that long non-coding RNAs (lncRNAs) are important in hepatocellular carcinoma (HCC) development and progression. In this study, we aim to evaluate the expression of lncRNA FAM99B and its biological function in HCC. METHODS: The expression level of FAM99B in HCC was assessed based on data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), verified using quantitative real-time polymerase chain reaction (qRT-PCR). HCCLM3 was transfected with lentivirus containing full-length FAM99B to obtain stable overexpressing cell line. Cell Counting Kit 8, clone formation, and transwell assays were used to investigate the effects of FAM99B in HCC progression. In addition, Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and PANTHER pathway analyses were conducted to investigate the underlying molecular mechanisms. RESULTS: FAM99B was found to be downregulated in HCC tissues compared with adjacent normal tissues based on TCGA, GEO, and qRT-PCR data. Our results revealed that downregulated FAM99B was significantly associated with vascular invasion, advanced histologic grade, and T stage. Kaplan-Meier analysis using TCGA data indicated that decreased FAM99B levels were significantly associated with poor overall survival in patients with HCC. Moreover, overexpression of FAM99B significantly inhibited cell proliferation, migration, and invasion in vitro. Pathway analyses showed that the co-expressed genes of FAM99B mainly participated in the pathways "Metabolic pathways" and "Blood coagulation". CONCLUSION: Our results suggest that FAM99B may serve as a tumor suppressor in HCC and may provide a promising therapy target for patients with HCC.
BACKGROUND: Increasing evidence has shown that long non-coding RNAs (lncRNAs) are important in hepatocellular carcinoma (HCC) development and progression. In this study, we aim to evaluate the expression of lncRNA FAM99B and its biological function in HCC. METHODS: The expression level of FAM99B in HCC was assessed based on data from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO), verified using quantitative real-time polymerase chain reaction (qRT-PCR). HCCLM3 was transfected with lentivirus containing full-length FAM99B to obtain stable overexpressing cell line. Cell Counting Kit 8, clone formation, and transwell assays were used to investigate the effects of FAM99B in HCC progression. In addition, Gene Ontology, Kyoto Encyclopedia of Genes and Genomes, and PANTHER pathway analyses were conducted to investigate the underlying molecular mechanisms. RESULTS:FAM99B was found to be downregulated in HCC tissues compared with adjacent normal tissues based on TCGA, GEO, and qRT-PCR data. Our results revealed that downregulated FAM99B was significantly associated with vascular invasion, advanced histologic grade, and T stage. Kaplan-Meier analysis using TCGA data indicated that decreased FAM99B levels were significantly associated with poor overall survival in patients with HCC. Moreover, overexpression of FAM99B significantly inhibited cell proliferation, migration, and invasion in vitro. Pathway analyses showed that the co-expressed genes of FAM99B mainly participated in the pathways "Metabolic pathways" and "Blood coagulation". CONCLUSION: Our results suggest that FAM99B may serve as a tumor suppressor in HCC and may provide a promising therapy target for patients with HCC.
Authors: Miriam Recalde; María Gárate-Rascón; José María Herranz; María Elizalde; María Azkona; Juan P Unfried; Loreto Boix; María Reig; Bruno Sangro; Maite G Fernández-Barrena; Puri Fortes; Matías A Ávila; Carmen Berasain; María Arechederra Journal: Cancers (Basel) Date: 2022-04-19 Impact factor: 6.575