Perezdrejer8953

Results 49 PTC patients with LNM and 15 without LNM were included in the present study. Exosomal miR-146b-5p and miR-222-3p were both significantly upregulated in patients with LNM (P values were 0.008 and 0.015, respectively). ROC analyses revealed that the areas under the curves (AUCs) of miR-146b-5p and miR-222-3p for LNM prediction were 0.811 and 0.834, respectively. Moreover, the AUC increased to 0.895 when the two miRNAs used together. Wound healing assays and transwell assays showed that miR-146b-5p and miR-222-3p significantly enhanced the migration and invasion ability of PTC cells in vitro. Conclusion Plasma exosomal miR-146b-5p and miR-222-3p could serve as potential biomarkers for LNM in PTC. © 2020 Jiang et al.Background KLF16, a member of the Kruppel-like factor (KLF) family, functions in the regulation of dopaminergic transmission, metabolism, and endocrinology. However, the role of KLF16 in prostate cancer (PCa) remains unknown. Methods We screened the expression of KLFs in PCa based on bioinformatics analysis. The protein levels of KLF16 in PCa specimens were confirmed by immunohistochemistry. Inhibiting KLF16 by RNA interference with shRNA was used to determine the effects of KLF16 on PCa cell growth in vitro and in vivo. RNA sequencing was used to investigate the signaling regulated by KLF16 in PCa. Bioinformatics analysis was also used to determine the possible correlations of KLF16 and signaling in PCa cohorts. Results Bioinformatics analysis showed that KLF16 may be required for PCa development. Notably, the expression of KLF16 was elevated in human PCa tissues. In vitro and in vivo experiments both demonstrated that depleting KLF16 significantly inhibited the growth of PCa cells. Downregulation of KLF16 significantly decreased the expression of MYC signaling in PCa cells. Furthermore, KLF16 expression was correlated with MYC signaling activity. Conclusion KLF16 was overexpressed in PCa tissues compared to normal tissues. KLF16 knockdown suppressed PCa cell growth in vitro and in vivo, and a deficiency of KLF16 inhibited activation of MYC signaling. © 2020 Zhang et al.Background Acute myeloid leukemia (AML) is a serious threat to human health. Long non-coding RNA (lncRNA) Taurine-Upregulated Gene1 (TUG1) has been reported to participate in the development and progression of several cancers, including AML. Herein, we aimed to investigate the pathognomonic role of TUG1 in AML cells and its potential mechanistic pathway. Methods Quantitative real-time PCR (qRT-PCR) assay was applied to detect the expression levels of lncRNA TUG1, miR-193a-5p and Rab10 in AML bone marrow and cell lines. The CCK-8 assay was conducted to assess the cell viability of AML HL-60 and NB4 cells and cell apoptotic assay was performed to assess the cell death. Dual-luciferase reporter assay was carried out to clarify the relationships among TUG1, miR-193a-5p and Rab10. Also, the protein level of Rab10 was examined by Western blot assay. Results LncRNA TUG1 was up-regulated in AML bone marrow and cells. Functional analysis showed that the silencing of TUG1 suppressed cell viability, while promoted cell death in AML HL-60 and NB4 cells. TUG1 targeted miR-193a-5p and negatively regulated miR-193a-5p expression. Overexpressed miR-193a-5p resulted in the decrease of cell viability and the increase in the cell death in AML cells. Restoration experiments proved that TUG1 regulated the cell viability and death of AML cells through regulating the miR-193a-5p/Rab10 axis. Rab10 was a direct target of miR-193a-5p and was inversely regulated by miR-193a-5p. TUG1 regulated the cell viability and death of AML cells through upregulating Rab10. Conclusion Silencing of lncRNA TUG1 induces a cytotoxic effect on AML cell lines through sponging miR-193a-5p and the suppression of Rab10. © 2020 Li and Wang.Purpose Although X-inactive specific transcript (XIST) is known to play a critical role in the pathogenesis of melanoma, the mechanisms through which this remains unclear. Methods RNAseq, immunohistochemistry, and qRT-PCR were used to identify the levels of XIST, miR-139-5p, and Rho-Associated Coiled-Coil Containing Protein Kinase-1 (ROCK1) in melanoma tissues and cells. A subcellular fractionation assay was used to determine the location of XIST. CCK-8 and colony formation assays were used to evaluate cellular proliferation. Cell migration and wound healing assays were used to detect the effects on cell migration. RNA pull-down was used to confirm the interaction between XIST and miR-139-5p. Besides, the xenograft tumor experiment was performed to further verify the roles of XIST in melanoma. Results In this study, an increased level of XIST was revealed in melanoma tissues and cells, which was associated with higher TNM stage and positive lymph node metastasis. XIST was found to function as a "molecular sponge" of miR-139-5p to facilitate cellular functions. Moreover, these consequences could be partially reversed by inhibition of miR-139-5p. Fumarate hydratase-IN-1 MiR-139-5p was found to target ROCK1 directly, leading to suppression of ROCK1 expression; this effect could be partially reversed by inhibiting XIST expression. Furthermore, the deletion of ROCK1 induced anti-oncogenic effects similar to those seen with knockout of XIST. Upregulation of miR-139-5p and knockdown of XIST could inhibit cell functions in melanoma. Conclusion Our findings suggested that the lncRNA XIST facilitates cellular functions in melanoma via the miR-139-5p/ROCK1 pathway. © 2020 Tian et al.Background Canonical Wnt/β-catenin signaling is frequently dysregulated in acute myeloid leukemia (AML) and has been implicated in leukemogenesis. γ-catenin was previously demonstrated to be associated with the nuclear localization of β-catenin, the central mediator, and to exert oncogenic effects in AML; however, the underlying mechanisms remain unclear. Our study aimed to investigate the expression characteristics of γ-catenin in AML patients, explore the mechanisms by which γ-catenin regulates β-catenin, and discuss the feasibility of targeting γ-catenin for AML treatment. Methods The mRNA expression levels of γ-catenin in AML patients were measured by qRT-PCR. Cell proliferation was examined via Cell Counting Kit-8 (CCK-8) assays. The expression levels of related proteins were measured via Western blotting. Specific siRNA was used to modulate the expression level of the γ-catenin gene. Apoptosis and cell cycle distribution were quantified by flow cytometry. The subcellular localization of γ-catenin and β-treatments. © 2020 Qian et al.Purpose Cervical cancer is one of the deadliest tumors among women in China. C-reactive protein (CRP), an indicator of inflammation, and lactate dehydrogenase (LDH), an enzyme ubiquitously expressed in cells, both play important roles in tumor growth and metastasis. Patients and Methods Based on pre-radiotherapy LDH and CRP median levels, we divided patients into four groups high LDH and CRP group, high LDH group, high CRP group, and low LDH and CRP group. Then, based on pre-/post-radiotherapy LDH and CRP ratios, we divided patients into four groups high LDH and CRP ratio group, high LDH ratio group, high CRP ratio group, and low LDH and CRP ratio group. Kaplan-Meier (KM) curves were constructed to show overall survival (OS). A multivariate Cox regression model was employed to identify the independent risk factors. Results High pre-radiotherapy LDH and CRP levels and increased pre-/post-radiotherapy LDH and CRP ratios were correlated with worst OS compared with the other three groups. Conclusion LDH and CRP were correlated with outcomes in patients with locally advanced cervical cancer. © 2020 Wang et al.Introduction Recently, the incidence of melanoma has been rising and there is a lack of effective targeted therapies. The regulatory mechanisms of microRNA-1246 (miR-1246) have been found in many cancers, except melanoma. This study focused on the regulatory mechanism of miR-1246 in melanoma development. Methods The expression of miR-1246 was assessed using quantitative real-time polymerase chain reaction (RT-qPCR). Cell viability and metastasis were detected by Transwell and MTT (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assays. The protein expression of epithelial mesenchymal transition (EMT) makers was assessed by Western blot analysis. The target gene of miR-1246 was detected using luciferase reporter assay. Results MiR-1246 expression was increased in melanoma tissues and cells. In addition, upregulation of miR-1246 promoted cell viability and metastasis in melanoma. Forkhead box protein A2 (FOXA2) was confirmed to be a direct target of miR-1246. And FOXA2 expression was decreased in melanoma and was suppressed by miR-1246. Importantly, upregulation of FOXA2 restored the carcinogenesis of miR-1246 in melanoma. Conclusion MiR-1246 promoted cell viability and metastasis in melanoma by inhibiting FOXA2 expression. © 2020 Yu et al.Aim Cullin 4B (CUL4B) is a member of the cullin ubiquitin-ligase family, which participates in proteolysis. Aberrant CUL4B expression has been shown in many malignancies. This study aimed to elucidate oncogenic role of CUL4B in gastric cancer (GC). Methods CUL4B expression in GC tissues was examined by RT-PCR and immunohistochemistry. The proliferation, invasion and tumorigenicity of GC cells with CUL4B overexpression or knockdown were evaluated. Results CUL4B expression significantly increased in GC tissues, and was correlated to UICC stage and differentiation of GC, as well as poor overall survival and disease-free survival. Both univariate and multivariate analysis identified CUL4B as an independent predictor for GC patient prognosis. In addition, CUL4B promoted GC cell proliferation and invasion in vitro and tumor formation in vivo. Conclusion CUL4B is overexpressed to promote GC development and progression. CUL4B is a promising prognostic marker and therapeutic target for GC. © 2020 Wu et al.Background Our previous study demonstrated that Id-1 may promote the tumorigenicity of esophageal squamous cell carcinoma (ESCC). Id-4 is another member of Id family, which is rare to be studied in ESCC. In this study, we investigated the expression of Id-4 in human ESCC specimens and determined whether Id-4 expression was associated with the clinicopathologic characteristic and the prognosis of ESCC patients. Methods We examined Id-4 expression using immunohistochemistry in 92 ESCC tissues and adjacent normal tissues. The association between Id-4 expression and clinical parameters and survival was evaluated by statistical analysis. Cox regression analyses were conducted to identify prognostic factors associated with overall survival (OS). In addition, we explored the functional mechanism of Id-4 in ESCC. Results Id-4 expression was significantly downregulated in ESCC tissues compared with adjacent normal tissues. The expression of Id-4 was associated negatively with pT stage (p=0.002), AJCC stage (p=0.008) athway. Thus, we believe that Id-4 may be a promising prognostic marker and a therapeutic target in ESCC. © 2020 Wang et al.Background 6-thioguanine (6-TG), as a conventional "ancient" drug for the treatment of acute leukemia, has been proved to have extensive anti-tumor roles. This study was created to investigate the hidden function of 6-TG on the MCF-7 breast cancer cell line (ER+, PR+) and its mechanisms. Methods MCF-7 cells were treated with 6-TG, and the IC50 value was measured by a cell counting kit-8 assay. Differentially expressed genes (DEGs) were confirmed by RNA-seq analysis. Apoptosis and cell cycle consequences were determined by flow cytometry and Western blot analyses. Results The results showed that colony formation decreased markedly and the percentage of cell apoptosis increased after 6-TG treatment. DNMT1 mRNA and protein expression decreased, and FAS expression increased. Moreover, 6-TG also induced MCF-7 cells to undergo G2/M phase cell cycle arrest and upregulated CDKN1A (p21). Conclusion Overall, our results suggest that 6-TG may induce FAS-mediated exogenous apoptosis and p21-dependent G2/M arrest by inhibiting the activity of DNMT1 in MCF-7 breast cancer cells.