作者机构：
[Liu, Ning; Liu, N; Xiang, Shuanglin; Hu, Xiang; Wei, Chenxi; Xiao, Ye; Ding, Xiaofeng] Hunan Normal Univ, Coll Life Sci, State Key Lab Dev Biol Freshwater Fish, Changsha 410081, Peoples R China.;[Liu, Ning; Long, Shengwen; Xun, Yu; Liu, N; Xiang, Shuanglin; Hu, Xiang; Huang, Shulan; Wei, Chenxi; Xiao, Ye; Chen, Wen; Ding, Xiaofeng; Qiu, Feng] Hunan Normal Univ, Coll Life Sci, State Educ Minist China, Key Lab Prot Chem & Dev Biol, Changsha 410081, Peoples R China.;[Liu, Ning] Hunan Normal Univ, Sch Med, Key Lab Study & Discovery Small Targeted Mol Huna, Changsha 410013, Peoples R China.;[Xiao, Ye] Cent S Univ, Xiangya Hosp, Endocrinol Res Ctr, Dept Endocrinol, Changsha 410008, Peoples R China.;[Sun, Yi] Cent S Univ, Xiangya Hosp 2, Dept Pathol, Changsha 410011, Peoples R China.
通讯机构：
[Liu, N; Xiang, SL; Liu, Ning] H;Hunan Normal Univ, Coll Life Sci, State Key Lab Dev Biol Freshwater Fish, Changsha 410081, Peoples R China.;Hunan Normal Univ, Coll Life Sci, State Educ Minist China, Key Lab Prot Chem & Dev Biol, Changsha 410081, Peoples R China.;Hunan Normal Univ, Sch Med, Key Lab Study & Discovery Small Targeted Mol Huna, Changsha 410013, Peoples R China.
关键词：
Hepatocellular carcinoma;Nuclear factor-kappaB;Protein kinase casein kinase II beta;Tumor necrosis factor alpha-induced protein 1;Tumor suppressor
摘要：
Background: Tumor necrosis factor alpha-induced protein 1 (TNFAIP1) is frequently downregulated in cancer cell lines and promotes cancer cell apoptosis. However, its role, clinical significance and molecular mechanisms in hepatocellular carcinoma (HCC) are unknown. Methods: The expression of TNFAIP1 in HCC tumor tissues and cell lines was measured by Western blot and immunohistochemistry. The effects of TNFAIP1 on HCC proliferation, apoptosis, metastasis, angiogenesis and tumor formation were evaluated by Cell Counting Kit-8 (CCK8), Terminal deoxynucleotidyl transferase dUTP Nick-End Labeling (TUNEL), transwell, tube formation assay in vitro and nude mice experiments in vivo. The interaction between TNFAIP1 and CSNK2B was validated by liquid chromatography-tandem mass spectrometry (LC-MS/MS), Co-immunoprecipitation and Western blot. The mechanism of how TNFAIP1 regulated nuclear factor-kappaB (NF-kappa B) pathway was analyzed by dual-luciferase reporter, immunofluorescence, quantitative Real-time polymerase chain reaction (RT-qPCR) and Western blot. Findings: The TNFAIP1 expression is significantly decreased in HCC tissues and cell lines, and negatively correlated with the increased HCC histological grade. Overexpression of TNFAIP1 inhibits HCC cell proliferation, metastasis, angiogenesis and promotes cancer cell apoptosis both in vitro and in vivo, whereas the knockdown of TNFAIP1 in HCC cell displays opposite effects. Mechanistically, TNFAIP1 interacts with CSNK2B and promotes its ubiquitin-mediated degradation with Cul3, causing attenuation of CSNK2B-dependent NF-kappa B trans-activation in HCC cell. Moreover, the enforced expression of CSNK2B counteracts the inhibitory effects of TNFAIP1 on HCC cell proliferation, migration, and angiogenesis in vitro and in vivo. Interpretation: Our results support that TNFAIP1 can act as a tumor suppressor of HCC by modulating TNFAIP1/CSNK2B/NF-kappa B pathway, implying that TNFAIP1 may represent a potential marker and a promising therapeutic target for HCC. (C) 2019 The Authors. Published by Elsevier B.V.
摘要：
the author names were incorrectly spelled as ** Linming Hu ** and ** Yinxing Tang **. The correct spelling are ** Linmin Hu ** and ** Yingxin Tang**. The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
通讯机构：
[Wei, Ke] H;Hunan Univ Chinese Med, Sch Med, Changsha, Hunan, Peoples R China.
摘要：
ABSTRACT Adjuvanted-influenza vaccination is an efficient method for enhancing the immunogenicity of influenza split-virus vaccines for preventing influenza. However, the medical community’s understanding of its performance in patients infected with HIV remains limited. To identify the advantages, we conducted a systematic review and meta-analysis with randomized controlled trials (RCTs) and cohort and case–control studies that have the immunogenicity and safety of influenza vaccines in patients infected with HIV as outcomes. We searched six different databases, and 1698 patients infected with HIV in 11 studies were included. Statistical analysis was performed to calculate the pooled standardized mean differences (SMD) or relative risk (RR) and 95% confidence interval (CI). Regarding immunogenicity, the pooled SMD of GMT (Geometric mean titer) for A/H1N1 was 0.61 (95%CI (0.40,0.82)), the pooled RR of seroconversion was 1.34 (95%CI (0.91,1.98)) for the H1N1 vaccine, 1.27(95%CI (0.64,2.52)) for the H3N2 vaccine, 1.19(95%CI (0.97,1.46)) for the B-type influenza vaccine. The pooled RR of seroprotection was 1.61 (95%CI (1.00,2.58)) for the H1N1 vaccine, 1.06 (95%CI(0.83,1.35)) for the H3N2 vaccine, and 1.13(95%CI(0.91,1.41)) for the B-type vaccine. Adjuvanted-influenza vaccination showed good general tolerability in patients infected with HIV, with the only significant increase being the rate of local pain at the injection site (RR = 2.03, 95%CI (1.06,3.86)). In conclusion, all studies evaluating injected adjuvanted influenza vaccination among patients infected with HIV showed acceptable levels of safety and immunogenicity.
作者机构：
[朱伟; 唐群; 刘春燕] Dept of Pathology, Hunan University of Chinese Medicine, Changsha, 410208, China;[杨胜辉] Dept of Preventive Medicine, Hunan University of Chinese Medicine, Changsha, 410208, China;[Zeng H.] Dept of Physiology, Hunan University of Chinese Medicine, Changsha, 410208, China;[魏科] Dept of Microbiology, Hunan University of Chinese Medicine, Changsha, 410208, China
摘要：
Combination with genomic DNA is one of the important ways for microRNAs (miRNAs) to perform biological processes. However, because of lack of an experimental method, the identified genomic sites targeted by microRNA were only located in the promoter and enhancer regions. In this study, based on affinity purification of labeled biotin at the 3'-end of miRNAs, we established an efficiently experimental method to screen miRNA binding sequences in the whole genomic regions in vivo. Biotinylated miR-373 was used to test our approach in MCF-7 cells, and then Sanger and next-generation sequencing were used to screen miR-373 binding sequences. Our results demonstrated that the genomic fragments precipitated by miR-373 were located not only in promoter but also in intron, exon, and intergenic. Eleven potentially miR-373 targeting genes were selected for further study, and all of these genes were significantly regulated by miR-373. Furthermore, the targeting sequences located in E-cadherin, cold-shock domain-containing protein C2 (CSDC2), and PDE4D genes could interact with miR-373 in MCF-7 cells rather than HeLa cells, which is consistent with our data that these three genes can be regulated by miR-373 in MCF-7 cells while not in HeLa cells. On the whole, this is an efficient method to identify miRNA targeting sequences in the whole genome.
