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Molecular Characteristics Models Determine Tractable Lead-like Phenyl-Piperazine Scaffolds as eIF4A1 ATP-competitive Inhibitors.
Univariate analysis revealed that lymphocytic thyroiditis, tumor size, number of CLNM, Level II LNM, Level III LNM, simultaneous Level II+III, simultaneous Level III+IV and simultaneous Level II+III+IV were significantly correlated with Level V LNM. In addition, multivariate analysis revealed that tumor size ≥2.5 cm, number of CLNM≥3, level II metastases and BRAFV600E mutation were independent Level V LNM predictors (odds ratio 3.910, 3.660, 8.410, 0.439; 95% CI 1.737-10.135, 1.054-12.713, 1.233-57.355, 0.280-0.827, respectively). Conclusion In summary, we presented several independent predictive factors for level V LNM in PTC patients. We constructed a risk prediction model consisting of tumor size ≥2.5 cm, number of CLNM≥3 and level II metastases and BRAFV600E mutation that may guide surgeons to evaluate the nodal status in PTC and perform tailored therapeutic LND.Background Long noncoding RNA has been involved in tumorigenesis of colorectal cancer (CRC). This study aimed to illustrate the functions and mechanisms of LINC00173 in CRC progression. Methods The expression of LINC00173 in CRC tissues and cell lines were analyzed via qRT-PCR. Kaplan-Meier curve was used to determine survival rate. Luciferase reporter assay was conducted to evaluate the interactions among LINC00173, miR-765 and PLP2 (proteolipid protein 2). CCK8 assay, EdU assay, transwell assay and xenograft assay were performed to examine the effect of LINC00173/miR-765/PLP2 axis on proliferation, migration and invasion. The Ki67 expression level in tumors tissues was detected through immunofluorescence assay. Results LINC00173 expression was markedly upregulated in CRC tissues and cells. High expression level of LINC00173 in CRC patients was correlated with poor prognosis. LINC00173 knockdown inhibited proliferation, migration, invasion and chemo-resistance of CRC cells in vitro. LINC00173 downregulation delayed CRC growth in vivo. LINC00173 interacted with miR-765 to promote PLP2 expression. Conclusion Our results demonstrated that LINC00173 plays an important oncogenic role in CRC via modulating miR-765/PLP2 axis. And LINC00173 may be a potential prognostic biomarker and therapeutic target for CRC.Purpose Long non-coding RNAs have been found to be involved in bladder cancer development. This article studied LINC00963 effects on bladder cancer progression to provide a novel treatment target. Patients and methods Totally 56 bladder cancer patients participated in this research. Bladder cancer cells were transfected. Cell counting kit 8 assay and clone formation experiment were used for cell viability and colony formation detection. Cell migration and invasion were determined by Transwell experiment. LINC00963 distribution was explored by cytoplasmic and nuclear extract isolation and quantitative real-time polymerase chain reaction. selleck chemicals Luciferase reporter experiment and RNA pulldown experiment were performed to detect the relationship between these two genes. The cancer genome atlas analysis was used for the detection of metastasis-associated protein 1 (MTA1) expression in bladder cancer. Results LINC00963 was seriously up-regulated in bladder cancer patients. High LINC00963 expression indicated high histological grade and low survival. LINC00963 was obviously up-regulated in bladder cancer cells. Knockdown of LINC00963 significantly reduced bladder cancer cells viability, colony formation, migration and invasion. Luciferase reporter experiment and RNA pulldown experiment revealed that LINC00963 promoted MTA1 expression via directly inhibiting miR-766-3p. MTA1 was up-regulated in bladder cancer patients. MTA1 up-regulation reversed the inhibitory effect of LINC00963 knockdown on bladder cancer cell viability, migration and invasion. Conclusion LINC00963 functions as an oncogene in bladder cancer by regulating the miR-766-3p/MTA1 axis.Background Epithelial-mesenchymal Transition (EMT) is involved in various cancers including glioblastoma. Our previous study has shown that miR-340 negatively correlated with EMT process in glioblastoma. Purpose In the present study, we aim to explore the underlying molecular mechanisms of miR-340 in EMT process of glioblastomas. Materials and methods Using RT-qPCR assay, we analyzed the expression of miR-340 in glioma cell lines and normal human glia (NHA) cell line. Using CCK8, Colony formation assays, transwell and Western blot assays, we investigated tumor growth and EMT process. Using luciferase reporter assay, we confirmed a target of miR-340. Results Our results showed that miR-340 was down-regulated in glioma cell lines (U87, U251 and LN229) compared to NHA cells. MiR-340 overexpression remarkably inhibited cell proliferation and invasion as well as up-regulated E-cadherin expression and down-regulated N-cadherin, Vimentin, ZEB1, Slug and Snail expressions in U251 and LN229 cells. Further studies have confirmed c-MET as a target gene of miR-340. The EMT-inhibitory effect of miR-340 was lost after c-MET expression was restored. We also identified the antitumorigenic activity of miR-340 in vivo. Conclusion These results demonstrated that miR-340 functioned as a tumor suppressor via targeting EMT process and could be a potential therapeutic candidate for treating glioblastomas.Objective To investigate the clinical safety, efficacy, therapeutic outcomes and risk factors of computed tomography-guided percutaneous cryoablation (CT-PCRA) for subcardiac hepatocellular carcinoma (HCC). Patients and methods In this study, patients with single HCC nodules located on the left lobe who subsequently underwent CT-PCRA were reviewed from July 2012 to August 2016. According to the definition of subcardiac HCC, the patients were grouped into the subcardiac HCC group (n=33) and the non-subcardiac HCC group (n=40). The technical success rates, tumour response rates, oncological outcomes including overall survival (OS) and recurrence-free survival (RFS) and complications were compared. Multivariate analysis was performed on clinicopathological variables to identify factors affecting long-term outcomes. Results Seventy-three patients with subcardiac HCC were included in this study. After a median follow-up time of 37.8 months, 27.4% (20/73) of the patients died. The technical success and complete response rates were not significantly different between the two groups (p = 1.
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