Pugholesen3612

The highest BRCA1 and 2 genetic mutation incidence is amongst the Chinese, but the Malays have the largest triple-negative breast cancer rates. These factors may also contribute to the statistical breast cancer data.MicroRNAs (miRs) modulate the expression of target genes in the signal pathway on transcriptome level. The present study investigated the 'epigenetic-based miRNA (epi-miRNA)-mRNA' regulatory network of miR-34b, miR-34c, miR-148a, miR-152, miR-200a and miR-200b epi-miRNAs and their target genes, DNA methyltransferase (DNMT1, 3a and 3b), phosphate and tensin homolog (PTEN) and NK3 Homeobox 1 (NKX3.1), in prostate cancer (PCa) using reverse transcription-quantitative PCR. The expression level of NKX3.1 were not significantly different between the PCa, Met-PCa and control groups. However, in the PCa and Met-PCa groups, the expression level of DNMT1 was upregulated, while DNMT3a, DNMT3b and PTEN were downregulated. Overexpression of DNMT1 (~5 and ~6-fold increase in the PCa and Met-PCa groups respectively) was accompanied by a decreased expression in PTEN, indicating a potential negative association. Both groups indicated that a high level of DNMT1 is associated with the aggressiveness of cancer, and there is a a directly proportional relationship between this gene and PSA, GS and TNM staging. A significant ~2 to ~5-fold decrease in the expression levels of DNMT3a and DNMT3b was found in both groups. In the PCa group, significant associations were identified between miR-34b and DNMT1/DNMT3b; between miR-34c/miR-148a and all target genes; between miR-152 and DNMT1/DNMT3b and PTEN; and between miR-200a/b and DNMT1. In the Met-PCa group, miR-148a, miR-152 and miR-200b exhibited a significant association with all target genes. A significant negative association was identified between PTEN and DNMT1 in the Met-PCa group. It was also revealed that that miR-148a, miR-152 and miR-200b increased the expression of DNMT1 and suppressed PTEN. Furthermore, the 'epi-miRNA-mRNA' bidirectional feedback loop was emphasised and the methylation pattern in PCa anti-cancer therapeutics was highlighted.The present study aimed to investigate expression of β2-adrenergic receptor (AR), the effect of the stress-related neurotransmitter norepinephrine (NE) on cell viability, proliferation and the therapeutic effect of propranolol, which is a typical β-blocker in various type of head and neck cancers for the first time. The β2-AR expression was investigated using immunohistochemistry and an immunoreactive scoring (IRS) system in 57 different head and neck cancer specimens, and reverse transcriptase-polymerase chain reaction and western blotting in four head and neck cancer cell lines (HNCCLs). Cell viability and proliferation assays were performed using 0, 1, 5 and 10 µM of NE and 1 µM of propranolol in four HNCCLs. The expression of β2-AR was positive in the majority of head and neck cancer tissues (55/57, 96.5%); however, it was significantly higher in oral cavity cancer than in pharyngeal cancer (median IRS 9 vs. 3; P less then 0.001). All HNCCLs exhibited β2-AR expression, with a higher expression level detected in the oral cavity cancer cell line than in the others. NE stimulated viability (oral cavity, 206%; larynx, 156%; pharynx, 130%; nasal cavity, 137%; 10 µM NE) and proliferation (124, 176, 131 and 127%, respectively) in a dose-dependent manner in all HNCCLs. Conversely, propranolol attenuated such viability (55, 42, 18 and 22%, respectively) and proliferation (22, 40, 61 and 48%, respectively). In conclusion, the viability and proliferation of various head and neck cancers may be directly stimulated by stress and this may be attenuated by β-blockers.Head and neck squamous cell carcinoma (HNSCC) has been associated with poor prognosis, due to its strong invasive ability and resistance to chemotherapy. Thus, there is an urgent requirement to identify effective biomarkers for the early diagnosis and prognostic evaluation of HNSCC. COP9 signalosome (COPS) regulates numerous cancer-associated biological processes in various malignancies. The aim of the present study was to investigate the association between COPS and HNSCC. The mRNA expression profiles of COPS in HNSCC were analyzed using UALCAN, Oncomine and UCSC Xena databases. The association between overall survival time in patients with HNSCC and the COPS genes was investigated using the Kaplan-Meier plotter database. The CERES score was obtained and evaluated to determine the importance of the COPS genes for survival of the HNSCC cell lines. Functional analysis for Gene Ontology and Gene Set Enrichment Analysis (GSEA) was performed using The Database for Annotation, Visualization and Integrated Discovery and GSEA software, respectively. After knocking down COPS5 and COPS6, cell Counting Kit-8 and wound healing assays were used to detect cell growth and migration of the CAL27 and SCC25 cell lines, respectively. Among the 10 COPS genes examined, most COPS subunits were upregulated in HNSCC samples compared with that in normal tissues, except for COPS9. Increased mRNA expression level of COPS5, COPS6, COPS7B, COPS8 and COPS9 was associated with TNM stage in patients with HNSCC. High mRNA expression level of COPS2, COPS5, COPS6, COPS7A, COPS7B, COPS8 and COPS9 had prognostic significance of patients with HNSCC. Knockdown of COPS5 and COPS6 inhibited cell growth and migration of the CAL27 and SCC25 cell lines. The results from the present study suggested that COPS subunits could be potential biomarkers in patients with HNSCC. COPS5 and COPS6 were important for cell survival and migration of the HNSCC cells.Laryngeal squamous cell carcinoma (LSCC) is a highly invasive malignant tumor in the head and neck area. As an oncogene, long non-coding RNA (lncRNA) nuclear enriched abundant transcript 1 (NEAT1) promotes cell proliferation, migration and invasion several types of cancer. The present study aimed to reveal the effects of NEAT1 on the progression of LSCC. Reverse transcription-quantitative PCR (RT-qPCR) was used to detect relative mRNA expression levels of NEAT1, microRNA (miR)-204-5p and semaphorin (SEMA) 4B. Kaplan-Meier analysis was used to analyze overall survival times. RNA in-situ hybridization (ISH) exhibited the distribution of NEAT1 and miR-204-5p in tissues. RNA fluorescence ISH was used to analyze the distribution of NEAT1 and miR-204-5p in the cells. Western blot analysis was used to detect the expression level of target proteins. Cell viability was analyzed using a MTT assay, while flow cytometry was used to determine cell apoptosis. Wound healing and Transwell invasion assays were used to value ce miR-204-5p/SEMA4B axis.The aim of the present study was to reveal the new molecular mechanism of long non-coding (lnc)RNA XIST in the development of hepatic carcinoma. A total of 69 patients with hepatic carcinoma were included. Hepatoma cell lines (SUN449), hepatoblastoma cell line (HepG2, Huh-6), liver cancer cell line (HepG2) and transformed human liver epithelial-2 cells (THLE-2) were used in the present study. A total 3 short hairpin RNA (sh)-lncRNA XIST sequences, overexpression vector (oe)-lncRNA XIST, microRNA (miR)-320a mimic, miR-320a inhibitor, PIK3CA inhibitor, and their corresponding controls were transfected in hepatic carcinoma cells. Reverse transcription-quantitative polymerase chain reaction was conducted to detect lncRNA-XIST, miR-320a and PIK3CA expression. Cell Counting Kit-8 assay and flow cytometry were undertaken to measure proliferation and apoptosis. see more Cell invasion and migration were detected by Transwell assays. Moreover, the binding of lncRNA XIST, PIK3CA and miR-320a were verified by luciferase reporter experiment and pull-down assay. Finally, a rescue assay was processed to confirm the effect of lncRNA-XIST, miR-320a and PIK3CA in the aforementioned processes. lncRNA XIST was highly expressed in hepatic carcinoma tissues and cells. The survival rate was significantly lower in the highly expressed lncRNA XIST group. shlncRNA XIST attenuated cell proliferation, invasion and migration, while increasing the apoptosis of hepatic carcinoma cells. The lncRNA XIST negatively targeted miR-320a, and miR-320a negatively regulated the expression of PIK3CA. The miR-320a mimic and PIK3CA inhibitor could recover the effect of oe-lncRNA in terms of the proliferation, invasion, migration and apoptosis of hepatic carcinoma cells. lncRNA XIST accelerates hepatic carcinoma progression by targeting the miR-320a/PIK3CA axis, which might provide the theoretical basis for the potential targeted therapy of hepatic carcinomas.[This retracts the article DOI 10.3892/ol.2021.12751.].A previous study has reported the oncogenic role of circular RNA (circ)-ATAD1 in gastric cancer. The aim of the present study was to investigate the role of circ-ATAD1 in acute myeloid leukemia (AML). Bone marrow mononuclear cells were collected from 60 patients with AML and 60 healthy controls, followed by RNA isolation and reverse transcription-quantitative PCR to assess the expression of circ-ATAD1 and microRNA (miR)-34b. A subcellular fractionation assay was used to determine the subcellular location of circ-ATAD1 in AML cells. Furthermore, circ-ATAD1 and miR-34b were overexpressed in AML cells to study crosstalk between the two molecules. The effect of circ-ATAD1 overexpression on miR-34b gene methylation was also analyzed by methylation-specific PCR, and the roles of circ-ATAD1 and miR-34b in the regulation of AML cell proliferation were analyzed by BrdU assay. circ-ATAD1 expression was found to be elevated, and inversely correlated with that of miR-34b, in patients with AML. Subcellular fractionation assays showed that circ-ATAD1 was specifically expressed in the nucleus. In addition, circ-ATAD1 overexpression in AML cells decreased miR-34b expression and increased miR-34b gene methylation. Moreover, AML cell proliferation was increased by circ-ATAD1 overexpression, but decreased by miR-34b overexpression, and the effect of circ-ATAD1 overexpression on AML cell proliferation was reduced by miR-34b overexpression. Together, these results indicate circ-ATAD1 as a nucleus-specific circRNA in AML, which promotes AML cell proliferation by downregulating miR-34b via methylation.Lung adenocarcinoma (LUAD) is the leading cause of cancer-related mortality worldwide. Long non-coding RNA (lncRNA) NUT family member 2A antisense RNA 1 (NUTM2A-AS1) is dysregulated in LUAD; however, its role in this disease remains unclear. The present study aimed to identify the underlying molecular mechanism of the effect of lncRNA NUTM2A-AS1 in LUAD by exploring whether lncRNA NUTM2A-AS1 could affect LUAD cell proliferation and apoptosis through the microRNA (miR)-590-5p/methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit (METTL3) axis. miR-590-5p was predicted and verified as the direct target of NUTM2A-AS1 using bioinformatics analysis and a dual luciferase reporter assay. The expression levels of NUTM2A-AS1 and miR-590-5p in lung cancer cells, and the effects of NUTM2A-AS1 on cell viability and apoptosis were determined using MTT assays and flow cytometry, respectively. Reverse transcription-quantitative PCR analysis revealed that the expression levels of NUTM2A-AS1 were significantly upregulated, while those of miR-590-5p were significantly downregulated, in lung cancer cells compared with the control epithelial cells.