Biological functions and molecular subtypes regulated by miR-142-3p in colon cancer.

MicroRNA-142-3p (miR-142-3p) has been reported to be implicated in colon cancer; however, the possible regulatory mechanisms and molecular subtypes regulated by miR-142-3p have not been fully elucidated. This study aimed to investigate the biological functions and regulatory mechanism of miR-142-3p in colon cancer. The expression level of miR-142-3p in colon cancer was analyzed based on the mRNA and miRNA expression datasets of colon cancer retrieved from The Cancer Genome Atlas. Target genes of miR-142-3p were also predicted. Based on these target genes, the functions and subtypes of miR-142-3p were investigated. The metabolic and tumor-related pathways, immune microenvironment, and target gene expression between the 2 subtypes were analyzed. MiR-142-3p was upregulated in tumor tissues, and its high expression indicated a poor prognosis. A total of 39 target genes were predicted, which were significantly involved in autophagy- and metabolism-related functions and pathways. Based on these target genes, the colon cancer samples were clustered into 2 subtypes. There were 35 metabolism-related pathways that were significantly different between the 2 clusters. The immune and stromal scores in cluster 2 were higher than those in cluster 1, whereas the tumor purity of cluster 2 was significantly lower than that of cluster 1. TP53INP2 expression in cluster 2 was higher than that in cluster 1. MiR-142-3p may promote colon cancer progression via autophagy- and metabolism-related pathways. MiR-142-3p may be served as a candidate target for the treatment of colon cancer.

TMEM88, CCL14 and CLEC3B as prognostic biomarkers for prognosis and palindromia of human hepatocellular carcinoma.

Hepatocellular carcinoma is one of the most mortal and prevalent cancers with increasing incidence worldwide. Elucidating genetic driver genes for prognosis and palindromia of hepatocellular carcinoma helps managing clinical decisions for patients. In this study, the high-throughput RNA sequencing data on platform IlluminaHiSeq of hepatocellular carcinoma were downloaded from The Cancer Genome Atlas with 330 primary hepatocellular carcinoma patient samples. Stable key genes with differential expressions were identified with which Kaplan-Meier survival analysis was performed using Cox proportional hazards test in R language. Driver genes influencing the prognosis of this disease were determined using clustering analysis. Functional analysis of driver genes was performed by literature search and Gene Set Enrichment Analysis. Finally, the selected driver genes were verified using external dataset GSE40873. A total of 5781 stable key genes were identified, including 156 genes definitely related to prognoses of hepatocellular carcinoma. Based on the significant key genes, samples were grouped into five clusters which were further integrated into high- and low-risk classes based on clinical features. TMEM88, CCL14, and CLEC3B were selected as driver genes which clustered high-/low-risk patients successfully (generally, p = 0.0005124445). Finally, survival analysis of the high-/low-risk samples from external database illustrated significant difference with p value 0.0198. In conclusion, TMEM88, CCL14, and CLEC3B genes were stable and available in predicting the survival and palindromia time of hepatocellular carcinoma. These genes could function as potential prognostic genes contributing to improve patients' outcomes and survival.

Long non-coding RNA HNF1A-AS1 promotes hepatocellular carcinoma cell proliferation by repressing NKD1 and P21 expression.

Hepatocellular carcinoma (HCC) is one of the most common cancers worldwide. Recent evidences have demonstrated that long non-coding RNAs (lncRNAs) act as key regulators of tumor development and progression including HCC. In the study, we showed that the expression level of HNF1A-AS1 was up-regulated in HCC cell lines. Furthermore, CCK-8 cell proliferation assays and cell cycle analysis showed that HNF1A-AS1 over-expression facilitated HCC cell proliferation by promoting the cell proliferation and S-phase progression, whereas HNF1A-AS1 knockdown had the opposite effect. Western-blotting analysis revealed that knockdown of HNF1A-AS1 inhibited the cycle-relative protein cyclin-D1 and PCNA expression in HCC cells. Mechanism, RNA immunoprecipitation (RIP) and Chromatin immunoprecipitation (ChIP) assays showed that by interacting with enhancer of zeste homolog 2 (EZH2), HNF1A-AS1 promoted HCC cell proliferation by repressing the NKD1 and p21 expression. These results suggested that HNF1A-AS1 may contribute to HCC progression, which may be an effective therapeutic target for patients.

Complete mitochondrial genome of the Nigeria-Cameroon chimpanzee, Pan troglodytes ellioti (Primates: Hominidae).

Chimpanzees are especially suited to teach us about ourselves, both in terms of their similarities and differences with human, and such important similarities and differences have also been noted for the incidence and severity of several major human diseases. In the present work, we report the entire mitochondrial genome of the Nigeria-Cameroon chimpanzee (Pan troglodytes ellioti) for the first time. Results shows that this mitogenome is 16,559 bp long and consists of 13 protein-coding genes, 22 transfer RNA genes, 2 ribosomal RNA genes, and 1 putative non-coding region (D-loop region). The genomic organization and gene order are the same as other Chimpanzees. The whole nucleotide base composition is 31.1% of A, 30.7% of C, 12.9% G, and 25.3% T, with a slight A+T bias of 56.4%. Most of the genes are encoded on H-strand, except for the ND6 subunit gene and 8 tRNA genes. The complete mitochondrial genome sequence reported here provides useful genetic information for P. t. ellioti, and will further contribute to the comparative genomics studies in primates.

[Effects of different doses of thrombopoietin on proliferation of bone marrow mesenchymal stem cells in mice].

To explore the effect of different doses of thrombopoietin on proliferation of bone marrow mesenchymal stem cells (MSCs) in mice, 20 Kunming mice (35 +/- 5 g) were divided randomly into 4 groups: low-dose TPO group, moderate-dose TPO group, high-dose TPO group and normal control group (n = 5). The experimental groups were subjected to intraperitoneal injections of TPO at a dose of 25, 50, 100 microg/kg, respectively, and normal control group were treated with saline at a dose of 0.1 ml/g per day for 5 days. The bone marrow was harvested on 12 hours after the final administration. The bone marrow nucleated cells (BMNCs) were counted and seeded at a density of 10(6) cells/cm(2). The colony-forming unit-fibroblast (CFU-F) of MSCs was cultured and evaluated. The CFU-F of MSCs underwent osteo-genic induction and adipogenic induction, and cytochemical and immunocytochemical staining were performed to verify their multipotential. CFU-F and the cell percentage of CD90(+), CD105(+), CD34(+) in BMNCs were analyzed by flow cytometry. The results showed that the number of BMNCs and the cell percentage of CD90(+), CD105(+), CD34(+) and CFU-F increased obviously in TPO groups as compared with the normal control group (p < 0.05). The number of BMNCs increased most obviously in the 50 microg/kg TPO group. However, there was no significant difference in number of CFU-F between 50 microg/kg and 100 microg/kg TPO group (p > 0.05). The CFU-F of MSCs in bone marrow had their osteogenic and adipogenic differentiation potentials in vitro. It is concluded that the number of BMNCs and the cell percentage of CD90(+), CD105(+) and CFU-F increased after administration with TPO. It means that TPO can enhance MSCs to proliferate in bone marrow. However, the number of BMNCs and CFU-F can not increase with the increase of TPO dose.

Evaluation of floc strength by morphological analysis and PDA online monitoring.

This paper established a method for the evaluation of floc strength by morphological analysis and PDA online monitoring. Theoretically, the binding force of a floc can be expressed as B=k(1)d(2Df/3), where k(1) is a coefficient, d is floc size and D(f) is the fractal dimension of the floc. In order to calculate the binding force under a given flocculation condition, a jar test was conducted and d and D(f) were measured by image analysis. A shear force was exerted on the grown flocs by introducing the flocculated suspension through a transparent tube where the velocity gradient value of the flow could be accurately controlled. As the tube was connected with a particle dispersion analyzer (PDA), the condition of floc breakage was online monitored and the critical condition was identified by analyzing the PDA outputs (FI curves). The binding force coefficient k(1) could thus be determined, and the binding force B which represented the floc strength was evaluated. The validity of this method was proved by a series of experiments using aluminium sulphate as coagulant for the flocculation of humic substances.