Long-chain non-coding RNA Linc00888 promotes the proliferation and migration of esophageal cancer cells by downregulating miR-34a expression.

OBJECTIVE: To explore the role and potential mechanism of long-chain non-coding RNA 00888 in esophageal cancer (EC). PATIENTS AND METHODS: The expression level of Linc00888 in esophageal cancer tissues and adjacent ones, as well as corresponding cell lines, was measured by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Survival prognosis information of patients was collected, and KM survival analysis was performed to determine the prognostic value of Linc00888. To better understand the effect of Linc00888 on the proliferative and migration ability of EC cells, Cell Counting Kit-8 (CCK-8), clone formation, and transwell assays were performed after Linc00888 was knocked down in EC cell lines. Furthermore, bioinformatics prediction website was used to discover the potential target of Linc00888. Then, Dual-Luciferase reporter gene assay was performed to verify the binding relationship between Linc00888 and the downstream gene miR-34a. Then, the expression relationship between the two was measured both in cell lines and tissues. Finally, to clarify the regulation between Linc00888 and miR-34a, a recovery experiment was performed using co-transfection technology. RESULTS: Linc00888 was aberrantly upregulated in esophageal cancer tissues. The survival analysis showed that the higher expression of Linc00888 was significantly correlated with shorter overall survival. Cell functional experiment results suggested that Linc00888 played a role in promoting tumor proliferative and migration ability in EC cells. Besides, Dual-Luciferase reporter genes assay indicated that miR-34a and Linc00888 had binding sites. Meanwhile, we confirmed that there was a negative correlation between the expression levels of miR-34a and Linc00888 in cells and tissues. Cellular functional recovery experiments revealed that Linc00888 could modulate the progression of EC by miR-34a. CONCLUSIONS: Linc00888 promotes the proliferative and migration ability of EC through miR-34a.

Large Isospin Asymmetry in

ß-delayed one-proton emissions of ^{22}Si, the lightest nucleus with an isospin projection T_{z}=-3, are studied with a silicon array surrounded by high-purity germanium detectors. Properties of ß-decay branches and the reduced transition probabilities for the transitions to the low-lying states of ^{22}Al are determined. Compared to the mirror ß decay of ^{22}O, the largest value of mirror asymmetry in low-lying states by far, with δ=209(96), is found in the transition to the first 1^{+} excited state. Shell-model calculation with isospin-nonconserving forces, including the T=1, J=2, 3 interaction related to the s_{1/2} orbit that introduces explicitly the isospin-symmetry breaking force and describes the loosely bound nature of the wave functions of the s_{1/2} orbit, can reproduce the observed data well and consistently explain the observation that a large δ value occurs for the first but not for the second 1^{+} excited state of ^{22}Al. Our results, while supporting the proton-halo structure in ^{22}Al, might provide another means to identify halo nuclei.

LncRNA HAGLR exacerbates hepatocellular carcinoma through negatively regulating miR-6785-5p.

OBJECTIVE: The purpose of this study was to explore the role of long non-coding RNA (lncRNA) HAGLR in exacerbating the development of hepatocellular carcinoma (HCC) by targeting microRNA-6785-5p (miR-6785-5p). PATIENTS AND METHODS: HAGLR levels in 46 HCC tissues and paracancerous tissues were detected. The relationship between HAGLR level and clinical features of HCC patients was analyzed. After knockdown of HAGLR, proliferative, and metastatic potential changes in Bel-7402 and Hub7 cells were assessed. Thereafter, the interaction between HAGLR and miR-6785-5p, as well as the involvement of miR-6785-5p in HAGLR-regulated HCC phenotypes were finally determined. RESULTS: It was found that HAGLR level was higher in HCC tissues than paracancerous ones and correlated with rates of lymphatic metastasis and distant metastasis but not with age, gender, and tumor staging in HCC patients. Survival analysis uncovered that HAGLR level was negatively linked to overall survival in HCC. After knockdown of HAGLR, proliferative, and metastatic potentials in Bel-7402 and Hub7 cells were attenuated. MiR-6785-5p was proven as the target gene binding to HAGLR. It was lowly expressed in HCC species, and negatively correlated with HAGLR level. Moreover, rescue experiments demonstrated that miR-6785-5p was responsible for HAGLR-regulated HCC phenotypes. CONCLUSIONS: LncRNA HAGLR stimulates proliferative and metastatic potentials in HCC via negatively regulating miR-6785-5p level, thus exacerbating the development of HCC.

LncRNA FAM83A-AS1 aggravates the malignant development of esophageal cancer by binding to miR-495-3p.

OBJECTIVE: It is of significance to screen out differentially expressed long non-coding RNAs (lncRNAs) that can be utilized as tumor biomarkers in esophageal cancer. This study aims to uncover the effect of lncRNA FAM83A-AS1 on regulating migratory potential in esophageal cancer and the underlying mechanism. PATIENTS AND METHODS: Tumor tissues and adjacent normal ones were collected from 62 esophageal cancer patients for detecting FAM83A-AS1 levels. Correlations of FAM83A-AS1 with clinical indexes and overall survival of esophageal cancer patients were analyzed. Thereafter, regulatory effects of FAM83A-AS1 on migratory potential in OE19 and OE33 cells were examined by transwell and wound healing assay. Then, the target genes of FAM83A-AS1 were predicted and functionally analyzed, and a protein interaction network was constructed. Finally, the mechanism of FAM83A-AS1 in regulating the downstream gene miR-495-3p was analyzed through Luciferase assay and rescue experiments. RESULTS: It was found that FAM83A-AS1 was upregulated in esophageal cancer tissues and cell lines. Higher rates of lymphatic and distant metastasis and worse survival were observed in esophageal cancer patients expressing higher level of FAM83A-AS1. Besides, the knockdown of FAM83A-AS1 suppressed migratory potential in OE19 cells, while the overexpression of FAM83A-AS1 yielded the opposite trend in OE33 cells. Moreover, miR-495-3p was indicated to be the target gene binding FAM83A-AS1, and it was lowly expressed in esophageal cancer and negatively regulated by FAM83A-AS1. Furthermore, the overexpression of miR-495-3p partially abolished the regulatory effect of FAM83A-AS1 on migratory potential in esophageal cancer. CONCLUSIONS: FAM83A-AS1 is upregulated in esophageal cancer, and it stimulates migratory potential in esophageal cancer by negatively regulating miR-495-3p.

The function and molecular mechanism of CEP55 in anaplastic thyroid cancer.

OBJECTIVE: The purpose of this study was to determine the role of centrosomal protein of 55 kDa (CEP55) in anaplastic thyroid cancer (ATC) and to further explore the mechanism, which might provide a new molecular marker for treatment of ATC. PATIENTS AND METHODS: The expression level of CEP55 in clinical cases was tested by fluorescence quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Also, qRT-PCR assay was performed in different TC cell lines. The relationship between CEP55 expression and clinicopathological characteristics was statistically analyzed. Kaplan-Meier curve and Cox's proportional hazards regression model were performed in survival analysis. Further, Western blot assay was used to analyze the protein expression changes in PI3K/Akt pathway. RESULTS: The expression level of CEP55 in TC tissues showed a noticeable upgrade, especially in ATC. In vitro, CEP55 expression was also increased in four kinds of TC cells, in which, the highest expression was found in ATC (TA-K) cells. The clinicopathological features, including lymph node metastasis, distant metastasis, and prognostic index were found to be correlated with the expression level of CEP55. Besides, the ATC patients with higher expression of CEP55 had a statistically worse overall survival (OS) time. In univariate analyses and multivariate analyses, the CEP55 level was an independent prognosis index of patients with ATC. In vitro study, CEP55 protein expression level was significantly reduced in si-CEP55-transfected TA-K cells. Notably, the downregulation of CEP55 could suppress the phosphorylation of PI3K and AKT. CONCLUSIONS: This study found that CEP55 could promote ATC progression, and PI3K/AKT pathway might be the downstream target of its action. These results provided a new therapeutic direction for the treatment of ATC.

Positive-Parity Linear-Chain Molecular Band in

An inelastic excitation and cluster-decay experiment ^{2}H(^{16}C,^{4}He+^{12}Be or ^{6}He+^{10}Be)^{2}H was carried out to investigate the linear-chain clustering structure in neutron-rich ^{16}C. For the first time, decay paths from the ^{16}C resonances to various states of the final nuclei were determined, thanks to the well-resolved Q-value spectra obtained from the threefold coincident measurement. The close-threshold resonance at 16.5 MeV is assigned as the J^{π}=0^{+} band head of the predicted positive-parity linear-chain molecular band with (3/2_{π}^{-})^{2}(1/2_{σ}^{-})^{2} configuration, according to the associated angular correlation and decay analysis. Other members of this band were found at 17.3, 19.4, and 21.6 MeV based on their selective decay properties, being consistent with the theoretical predictions. Another intriguing high-lying state was observed at 27.2 MeV which decays almost exclusively to ^{6}He+^{10}Be(∼6 MeV) final channel, corresponding well to another predicted linear-chain structure with the pure σ-bond configuration.

The recovery effect of proanthocyanidin on microtensile bond strength to sodium hypochlorite-treated dentine.

AIM: To evaluate the recovery effect of proanthocyanidin (PA) on microtensile bond strength (µTBS) to sodium hypochlorite (NaOCl)-treated dentine. METHODOLOGY: Fifty-five freshly extracted third molars with intact dental crowns, no caries or restorations were sectioned to expose a sound middle layer of dentine and were randomly divided into 11 groups. In the blank control group, dentine surfaces were immersed in deionized water for 20 min. In the negative control group, dental surfaces were immersed in 5.25% NaOCl for 20 min. In the other nine experimental groups, after immersion for 20 min in 5.25% NaOCl, followed by PA (5%, 10%, or 15%) treatment for 1, 5 min or 10 min. The NaOCl solution was renewed every 5 min. Then dentine surfaces were bonded using SE bond. Bonded samples were sectioned into dentine-resin sticks (n = 45) for microtensile bond strength testing (MPa). Failure modes were observed and classified into three types with a stereomicroscope. Microtensile bond strength data were analysed using one-way anova. The confidence interval test was performed to analyse the recovery effect of PA on bond strength to NaOCl-treated dentine. The chi-squared test was used to analyse failure mode distribution. RESULTS: After use of 5.25% NaOCl for 20 min, microtensile bond strength in the negative control group decreased significantly compared with that of the untreated group (P < 0.05). After a recovery treatment of 10% PA for 10 min or 15% PA for more than 5 min, the bond strength was restored to at least 90% of baseline (P < 0.05). No recovery effect on bond strength was detected after the application of 5% PA for 1 min (P > 0.05). Adhesive fracture was found to be the most common failure mode in the NaOCl-treated group. After the recovery application of PA, the proportion of mixed failures increased significantly (P < 0.05). CONCLUSIONS: Microtensile bond strength to NaOCl-treated dentine recovered after the application of either 5% PA for more than 5 min or 10% or 15% PA for more than 1 min. The application of PA before an adhesive procedure may immediately restore the compromised bond strength of NaOCl-treated dentine.

[Cleaning efficacy of different solvents on sealer-contaminated dentin surface].

OBJECTIVE: To evaluate the influence of an epoxy resin-based sealer on the bond strength of adhesive resins to dentin and the cleaning efficacy of different solvents in removing sealer residues. METHODS: The occlusal enamel of 25 freshly extracted human third molars without caries were removed to expose flat surfaces of dentin. The teeth were randomly divided into five groups according to the treatment received: For negative control group, the dentin surfaces were not contaminated with AH-Plus; For the other 4 experimental groups, the samples were contaminated with AH-Plus for 5 min and different measures were taken: For positive control group, the sealer were wiped with dry cotton pellets; For solvents experimental groups: cotton pellets saturated with 95% (volume fraction) ethanol, 99.5% (volume fraction) acetone or 99% (volume fraction) amyl acetate were used to wipe the sealer until the surface appeared clean when viewed through a stereomicroscope under ×10 magnification, then rinsed with de-ionized water for 3 s. After sealer removal, a self-etching adhesive system was applied on the surfaces with resin composite. The samples were sectioned into 1.0 mm×1.0 mm stick specimens (n=45) for microtensile test. Failure modes at the dentin-resin interface were observed using a stereomicroscope. The samples were sectioned into 1.0 mm piece specimens (n=4) for scanning electron microscope observation. The microtensile bond strength data were analyzed by one-way ANOVA. Chi-square test were used to analyse the failure modes between the groups. RESULTS: There was significant difference among the five groups (P<0.001). For dry cotton pellet group (38.69±8.60) MPa and the ethanol group (37.14±12.01) MPa, the microtensile bond strength significantly declined when compared with negative control group (43.86±7.99) MPa (P<0.05). No significant difference of bond strength was found between the dry cotton pellet group and the ethanol group (P=0.426). There was no statistical significant difference among acetone group, amyl acetate group and negative control group (P>0.05). The bond strength of acetone group and amyl acetate group were (45.94±10.37) MPa and (43.99±7.01) MPa, respectively. The ethanol group exhibited lower bond strength than that of acetone group and amyl acetate group (P<0.05). Scanning electronic microscope observation revealed that in dry cotton pellet group and ethanol group, the resin tags were short and loose. Moreover, sealer residues were identified in the interface in the ethanol group samples, while the resin tags in the acetone and amyl acetate group were as dense and uniform as in negative control group. The distribution of failure modes showed no significant difference in the five groups (P=0.086). CONCLUSION: The microtensile bond strength of dentin to composite resin was lower after exposure to sealer. Compared with ethanol and dry cotton pellets, the cleaning effect of acetone and amyl acetate on sealer-contaminated dentin surface were better.