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Hepatocellular carcinoma (HCC) is among the most common types of cancer that threat the public health worldwide. N6-methyladenosine (m6A) RNA methylation is associated with cancer initiation and progression, and is dynamically regulated by m6A RNA methylation-associated genes. However, little is known about the expression status and the prognostic value of m6A-associated genes in HCC. The present study aimed to identify the expression profiling pattern and clinical significance of m6A-associated genes in HCC. Consensus clustering analysis was performed to identify the clusters of HCC with different clinical outcomes. A prognostic signature built by the least absolute shrinkage and selection operator Cox regression model was utilized to discover subtypes associated with different clinical outcomes of patients with HCC in the discovery cohort from The Cancer Genome Atlas. The differences between subgroups were characterized in terms of epigenetic dysregulation and somatic mutation frequencies. The International Cancer Genome Consortium cohort and two independent cohorts from the meta-Gene Expression Omnibus database were used for external validation. Most of the m6A-associated genes were upregulated and involved in the prognosis and malignancy of HCC. A four-gene prognostic signature revealed two HCC subtypes (namely, high- and low-risk group) that was associated with different clinical outcomes. Patients in the high-risk group were accompanied with increased epigenetic silencing and significant mutations in TP53 and FLG, while ALB was frequently mutated in the low-risk group. In conclusion, an m6A-based signature was constructed to predict the prognosis of patients with HCC, which may provide a tool for reliable prognosis assessment for clinicians, and aid clinical treatment decision-making.Recent studies have demonstrated that circular RNAs (circRNAs) play an important role in the development of gastric cancer (GC). The present study aimed to investigate the role of hsa_circ_0076305 (circPGC) in GC. The levels of circRNAs and mRNAs in AGS cell lines were detected via reverse transcription-quantitative PCR, and western blotting was performed to detect protein expression levels. Functional studies were explored by CCK8 assay and cell migration assay. Functional studies have indicated that circPGC orchestrates two cellular processes; it inhibits proliferation, and promotes migration and invasion in the GC AGS cell line, a phenomenon called ‘migration-proliferation dichotomy’, as well as epithelial-to-mesenchymal transition in AGS cells. In addition, circPGC degrades the extracellular matrix and basement membrane through matrix metallopeptidase (MMP)9 and MMP14, providing a microenvironment that facilitates cell migration. The results also demonstrated that circPGC expression is lower in clinical patients with later stages of GC, which is associated with poor prognosis. Taken together, these results suggest that circPGC exhibits migration-proliferation dichotomy during GC development, invasion and migration.[This retracts the article DOI 10.3892/ol.2018.8086.].In the era of immunochemotherapy, the traditional international prognostic index (IPI) has partially lost its predictive value in diffuse large B-cell lymphoma (DLBCL) and the National Comprehensive Cancer Network-IPI (NCCN-IPI) is unable to effectively identify high-risk patients. Thus, the present study aimed to develop a modified prognostic model (M-PM) to identify high-risk patients that require aggressive treatment. The present study included 169 patients with newly diagnosed DLBCL treated with rituximab, cyclophosphamide, doxorubicin, vincristine and prednisone (RCHOP) or RCHOP-like regimens, between 2011-2017. The results demonstrated that the risk discrimination was improved in the NCCN-IPI compared with the IPI, and patients were divided into four risk groups with a 5-year overall survival rate of 93.8, 76.5, 54.3 and 39.4%, respectively. However, the NCCN-IPI failed to identify the high-risk DLBCL population. The newly developed M-PM presented here included four parameters Age (≥65 years), an elevated lactate dehydrogenase level, Eastern Cooperative Oncology Group score ≥2 and total metabolic tumor volume ≥300 cm3. The M-PM also divided patients into four risk groups that comprised 40.8, 23.1, 26.0 and 10.1% of the patients, and the 5-year survival rates of these groups were 92.4, 70.6, 52.3 and 24.5%, respectively. Taken together, the results of the present study demonstrated that the M-PM was more accurate compared with the IPI and the NCCN-IPI, which served as an effective tool for identifying patients with DLBCL at high risk of an adverse prognosis.Osteosarcoma (OS) is the most common primary malignant tumor of bone. It is a common phenomenon that osteosarcoma cells have a hypoxic microenvironment. Hypoxia can dedifferentiate cells of several malignant tumor types into stem cell-like phenotypes. However, the role of hypoxia in stemness induction and the expression of cancer stem cell (CSC) markers in human osteosarcoma cells has not been reported. The present study examined the effects of hypoxia on stem-like cells in the human osteosarcoma MNNG/HOS cells. Oxaliplatin Under the incubation with 1% oxygen, the expression of CSCs markers (Oct-4, Nanog and CD133) in MNNG/HOS cells were increased. Moreover, MNNG/HOS cells cultured under hypoxic conditions were more likely to proliferate into spheres and resulted in larger xenograft tumor. Hypoxia also increased the mRNA and protein levels of hypoxia-inducible factor (HIF)-1α. Then rapamycin was used, which has been shown to lower HIF-1α protein level, to inhibit the hypoxic response. Rapamycin suppressed the expression of HIF-1α protein and CSCs markers (Oct4, Nanog and CD133) in MNNG/HOS cells. In addition, pretreatment with rapamycin reduced the efficiency of MNNG/HOS cells in forming spheres and xenograft tumors. The results demonstrated that hypoxia (1% oxygen) can dedifferentiate some of the MNNG/HOS cells into stem cell-like phenotypes, and that the mTOR signaling pathway participates in this process via regulating the expression of HIF-1α protein.