Huntington’s disease (HD) is a neurodegenerative disease. MicroRNAs (miRNAs) are small non-coding RNAs that mediate post-transcriptional regulation of target genes. Although miRNAs are extensively edited in human brains, the editome of miRNAs in brains of HD patients is largely unknown. By analyzing the small RNA sequencing profiles of brain tissues of 28 HD patients and 83 normal controls, 1182 miRNA editing sites with significant editing levels were identified. In addition to 27 A-to-I editing sites, we identified 3 conserved C-to-U editing sites in miRNAs of HD patients. 30 SNPs in the miRNAs of HD patients were also identified. Furthermore, 129 miRNA editing events demonstrated significantly different editing levels in prefrontal cortex samples of HD patients (HD-PC) when compared to those of healthy controls. We found that hsa-mir-10b-5p was edited to have an additional cytosine at 5’-end in HD-PC, and the edited hsa-mir-10b repressed GTPBP10 that was often downregulated in HD. The down-regulation of GTPBP10 might contribute to the progression of HD by causing gradual loss of function of mitochondrial. These results provide the first endeavor to characterize the miRNA editing events in HD and their potential functions.

Ovarian cancer is a kind of cancer from the female genital tract; the molecular mechanism still needs to be explored. lncRNA plays a vital role in tumorigenesis and development. Our aim was to identify oncogenic lncRNAs in ovarian cancer and explore the potential molecular mechanism. SNHG15 was initially identified by using GEO datasets (GSE135886 and GSE119054) and validated by tumor tissues and the cell line, identifying that SNHG15 was upregulated in ovarian cancer. Besides, high SNHG15 indicated poor prognosis in ovarian cancer. Furthermore, knockdown SNHG15 suppresses ovarian cancer proliferation and promotes apoptosis. Mechanistically, SNHG15 promotes proliferation through upregulated CDK6 via sponging miR‐370‐3p. Taken together, our findings emphasize the important role of SNHG15 in ovarian cancer, suggesting that SNHG15 may be a promising target for ovarian cancer.

Background. Hsp70 (heat shock protein 70) plays a key role in carcinogenesis and cancer progression. However, the relationship between the Hsp70 expression level and the colorectal cancer patient survival is unknown. This study is aimed at investigating the relationship between Hsp70 and the prognosis of colorectal carcinoma patients. Methods. PubMed, Web of Science, and Embase were used for systematic computer literature retrieval. Stata SE14.0 software was used for quantitative meta‐analysis. Besides, data was extracted from selected articles. Relationships between Hsp70 expression level and prognosis were further studied. The hazard ratios (HRs) and 95% confidence intervals (95% CIs) were also computed. Results. A total of 11 potentially eligible studies with 2269 patients were identified in 10 tumors from PubMed, Web of Science, and Embase. Hsp70 overexpression was associated with poor overall survival (OS) and disease‐free survival (DFS) in colorectal carcinoma patients (HRs, 0.65 (95% CI: 0.52‐0.78) and 0.77 (95% CI: 0.23‐1.32), respectively). Conclusions. Hsp70 overexpression can predict poor survival in colorectal cancer patients.

Background: Proliferation-associated nucleolar protein p120 (NOP2) has been proven to be a promising tumor cell maker, but it has not been specifically studied in colon cancer. This study aims to investigate the role and action mechanism of NOP2 in colon cancer. Methods: Fluorescence quantitative PCR and western blot assays were used to evaluate the expression of NOP2. NOP2 siRNA was transfected into HCT116, LOVO, and CCK-8 cells, and transwell assays were performed to evaluate the cell proliferation, migration, and invasion. Transcriptome sequencing of both the NOP2 knockdown and negative control (NC) groups was performed. Results: NOP2 expression is significantly upregulated in colon cancer tissues and cells compared with that in the healthy controls. The proliferation, migration, and invasion of the colon cancer cells were significantly suppressed in the NOP2 knockdown group compared with those in the NC group (P<0.05). Transcriptome sequencing showed that ASMTL and C6orf52 were significantly downregulated, while MUC19, TXK, APOBEC2, and RBM44 were upregulated in both of the two NOP2 silenced colon cancer cells relative to those in the control. Gene Ontology (GO) analysis showed that NOP2 knockdown mainly induced differential expression of the genes involved in positive regulation of T cell-mediated cytotoxicity and thiamine metabolism. Kyoto Encyclopedia of Genes and Genomes analysis showed that the gene pathways most significantly affected by NOP2 knockdown were Cytokine-cytokine receptor interaction, Type I diabetes mellitus, Taste transduction, and Systemic lupus erythematosus. Conclusions: NOP2 promotes proliferation, migration, and invasion of colon cancer cells, and the underlying mechanisms may be related to TXK tyrosine kinase.

Cancer is one of the main causes of human death worldwide. Recently, many studies have firmly established the causal relationship between oxidative stress and cancer initiation and progression. As a key protein in PI3K/Akt signaling pathway, p-AKT (phosphorylated Akt) participates in the process of oxidative stress and plays a prognostic role in various hematologic tumors and solid tumors. We conducted a comprehensive search of the PubMed, Embase and Cochrane libraries to identify studies published in the past decade involving cancer patients expressing p-AKT that reported overall survival (OS) during follow-up. In this study, 6,128 patients in total were evaluated from 29 enrolled articles, and we concluded that overexpression of p-AKT was closely related to worse OS in cancer patients with a hazard ratio (HR) of 2.33 (95% CI: 1.67–4.00). Furthermore, we conducted a subgroup analysis, and the results indicated that overexpression of p-AKT was associated with worse OS in hematological tumor (HR: 1.64, 95% CI: 1.41–1.92), and solid tumor (HR: 2.44, 95% CI: 1.61–5.26). High expression of p-AKT is related to poor prognosis of various hematologic tumors and solid tumors.

Background: The relationship between interleukin-8 (IL-8) expression and the prognosis of gastric cancer (GC) patients has been reported, but the results are contradictory.Aim: To investigate the effect of IL-8 expression on the prognosis of patients with GC.Method: A comprehensive search strategy was used to search the PubMed, Web of Science and Cochrane Library databases. The total survival time was analysed using the RevMan 5.4 software. Through extensive search and meta-analysis of relevant studies, studies examining the relationship between IL-8 expression and prognosis in patients with GC were conducted to obtain more accurate estimates.Findings: Eight studies (1843 patients) were included. The combined results of all the studies showed that high expression of IL-8 was a risk factor for poor prognosis in patients with GC (hazard ratio (HR): 2.08; 95% CI: 1.81–2.39). Sensitivity analysis suggested that the pooled HR was stable, and omitting a single study did not change the significance of the pooled HR. Funnel plots revealed no significant publication bias in the meta-analysis.Conclusion: High IL-8 expression could be a negative prognostic biomarker for patients with GC.