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lncRNA UASR1 (UASR1) has been characterized as an oncogenic lncRNA in breast cancer. UASR1 was predicted to interact with miR-107, which serves tumor suppressive roles mainly by targeting CDK8. The present study was performed to investigate the interactions among UASR1, miR-107 and CDK8 in colorectal cancer (CRC). A total of 62 patients with CRC, including 40 males and 22 females (age range, 38-67 years; mean age, 57.2±7.6 years) were enrolled at the Second Hospital of Shandong University between July 2012 and July 2014. The expression of UASR1 in tissues and cells were detected by reverse transcription-quantitative polymerase chain reaction. The interaction between UASR1 and miR-107 was investigated by performing dual luciferase activity assay, and the effects of overexpression of UASR1, miR-107 and CDK8 on the proliferation of CR4 cells were analyzed by performing cell proliferation analysis. It was observed that UASR1 is upregulated in CRC and its high expression levels predicted poor survival in patients with CRC. RNA-RNA interaction prediction demonstrated that UASR1 may interact with miR-107. In CRC cells, overexpression of UASR1 and miR-107 did not affect each other. However, the expression of CDK8, a target of miR-107, was upregulated following overexpression of UASR1. Notably, overexpression of UASR1 decreased the inhibitory effects of miR-107 on cell proliferation and the expression of CDK8. Therefore, UASR1 may sponge miR-107 to upregulate oncogenic CDK8, thereby promoting CRC cell proliferation.Cutaneous T cell lymphomas (CTCLs) are a group of heterogeneous, life-threatening, extra-nodal and lymphoproliferative T cell neoplasms. Since chronic inflammation serves a key role in CTCL progression, curcumin, a natural pigment with proven anti-inflammatory and antineoplastic properties, as well as minimal toxicity, may be used as a therapeutic agent. In the present study, two formulations of curcumin (standard ethanolic and a Pluronic®P-123/F-127 micellar solution) were compared regarding their cytotoxic efficacy and speed of internalization in three CTCL cell lines, namely HuT-78, HH and MJ. In addition, the modulating effect of curcumin on selected proteins involved in the proliferation and progression of the disease was determined. The results indicated the superiority of the Pluronic®P-123/F-127 micellar curcumin over the standard ethanol solution in terms of cellular internalization efficiency as determined by spectrophotometric analysis. Notably, the presence of commonly used media components, such as phenol red, may interfere when interpreting the cytotoxicity of curcumin, due to their overlapping absorbance peaks. Therefore, it was concluded that phenol red-free media are superior over media with phenol red in order to correctly measure the cytotoxic efficacy and cell penetration of curcumin. Depending on the cell line, the IC50 values of micellar curcumin varied from 29.76 to 1.24 µΜ, with HH cells demonstrating the highest sensitivity. This cell line had the lowest expression levels of the Wilms' tumor-1 transcription factor. Performing western blot analyses of treated and untreated CTCL cells, selective signal transduction changes were recorded for the first time, thus making curcumin nano-formulation an attractive and prospective option with therapeutic relevance for CTCL as a rare orphan disease.Malignant tumor cells are able to transdifferentiate into other cell types in various tissues or organs. Recent studies have demonstrated the ability of cancer cells to transdifferentiate into functional endothelial cells (ECs). PAI039 However, whether human gastric cancer (GC) cells are able to transdifferentiate into other cell types has remained largely elusive. Furthermore, whether HGC-27 cells are able to participate in GC angiogenesis remains to be clarified. In the present study, the HGC-27 cell line grown under hypoxic conditions for 4 days exhibited the typical 'flagstone' appearance, which is typical for cultured ECs. HGC-27 cells cultured on Matrigel under hypoxic conditions gradually formed net-like structures. Furthermore, the cultured HGC-27 cells expressed CD31, CD34 and von Willebrand factor, the molecular markers for ECs, under hypoxic conditions. These results indicated that HGC-27 cells, cultured under hypoxic conditions, are able to transdifferentiate into EC-like cells in vitro.Areca nut chewing is an important risk factor for developing tongue squamous cell carcinoma (TSCC), although the underlying molecular mechanism is unknown. To determine the potential molecular mechanisms of areca nut chewing-induced TSCC, the present study performed whole-genome detection with five pairs of TSCC and adjacent normal tissues, via mRNA- and long non-coding (lnc)RNA-gene chip analysis. A total of 3,860 differentially expressed genes were identified, including 2,193 lncRNAs and 1,667 mRNAs. Gene set-enrichment analysis revealed that the differentially expressed mRNAs were enriched in chromosome 22q13, 8p21 and 3p21 regions, and were regulated by nuclear factor kappa B (NF-κB) and interferon regulatory factors (IRFs). The results of ingenuity pathway analysis revealed that these mRNAs were significantly enriched for inflammatory immune-related signaling pathways. A co-expression network of mRNAs and lncRNAs was constructed by performing weighted gene co-expression network analysis. The present study focused on NF-κB-, IRF- and Th cell-signaling pathway-related lncRNAs and the corresponding mRNA-lncRNA regulatory networks. To the best of our knowledge, the present study was the first to investigate differential mRNA- and lncRNA-expression profiles in TSCCs induced by areca nut chewing. Inflammation-related mRNA-lncRNA regulatory networks driven by IRFs and NF-κB were identified, as well as the Th cell-related signaling pathways that play important carcinogenic roles in areca nut chewing-induced TSCC. These differentially expressed mRNAs and lncRNAs, and their regulatory networks provide insight for further analysis on the molecular mechanism of areca nut chewing-induced TSCC, candidate molecular markers and targets for further clinical intervention.
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