Retracted: Resveratrol Suppresses Human Nasopharyngeal Carcinoma Cell Growth Via Inhibiting Differentiation Antagonizing Non-Protein Coding RNA (DANCR) Expression.

The authors have requested retraction due to the identification of errors in the data. Reference: Jiafeng Zhang, Xiaojie Jin, Chuan Zhou, Hui Zhao, Ping He, Yalin Hao, Qiongna Dong. Resveratrol Suppresses Human Nasopharyngeal Carcinoma Cell Growth Via Inhibiting Differentiation Antagonizing Non-Protein Coding RNA (DANCR) Expression. Med Sci Monit, 2020; 26: e923622. DOI: 10.12659/MSM.923622.

Resveratrol Suppresses Human Nasopharyngeal Carcinoma Cell Growth Via Inhibiting Differentiation Antagonizing Non-Protein Coding RNA (DANCR) Expression.

BACKGROUND Although resveratrol has been found to show anti-cancer effects and potential chemotherapeutic activities in several cancers, the role and molecular mechanisms of resveratrol in nasopharyngeal carcinoma (NPC) remains poorly understood. This study aimed to investigate the effect of resveratrol in NPC progression and its molecular mechanism. MATERIAL AND METHODS Quantitative real-time polymerase chain reaction and western blotting were used to detect the expression of DANCR and PTEN. MTT assay and EdU assay were performed to detect the cell proliferation in NPC cells with different treatment. The effect of resveratrol on cell migration was explored by Transwell migration assay. RNA immunoprecipitation assay and chromatin immunoprecipitation assay were performed to test the interaction between DANCR, EZH2, and PTEN. A mouse xenograft model of NPC cell was established, and immunohistochemistry assay was performed to detect the PTEN expression. RESULTS Resveratrol treatment inhibited NPC cell growth and migration in a dose-dependent manner. Additionally, resveratrol downregulated the expression of DANCR and DANCR overexpressing abrogated the inhibition effect of resveratrol on NPC cell migration. Mechanistically, DANCR could bind to EZH2 and downregulated PTEN expression through mediating the binding of EZH2 on PTEN promoter. Furthermore, rescue experiments suggested resveratrol inhibited NPC cell growth and migration by the DANCR/PTEN pathway. Resveratrol significantly decreased the tumor volume and tumor weight and increased the expression of PTEN. CONCLUSIONS Resveratrol increased PTEN expression and suppressed NPC cell growth and migration through downregulation of DANCR.

Long non­coding RNA DANCR promotes nasopharyngeal carcinoma cell proliferation and migration.

Aberrant expression of numerous long non­coding RNAs (lncRNAs) has been reported to be associated with nasopharyngeal carcinoma (NPC). The present study aimed to investigate the expression and function of lncRNA differentiation antagonizing non­protein coding RNA (DANCR) in NPC pathogenesis. Reverse transcription­quantitative polymerase chain reaction results suggested that DANCR was significantly upregulated in NPC cells. Overexpression of DANCR promoted 5­8F cell proliferation and migration, as detected by Cell Counting Kit­8, colony formation and wound healing assays. DANCR was additionally identified to inhibit apoptosis, as determined by flow cytometric analysis. Furthermore, DANCR knockdown suppressed cell proliferation and migration, and promoted cell apoptosis in SUNE­1 cell. Western blot analysis suggested that DANCR regulated the phosphorylation of AKT serine/threonine kinase and the protein expression of PTEN in NPC cells. Knockdown of DANCR decreased tumor growth in a xenograft model following subcutaneous injection of SUNE­1 cells. Collectively, the present results suggested that DANCR regulated the proliferation, migration and apoptosis of NPC cells.

[Expression and clinical significance of Muc1, p63 protein in diffuse sclerosing variant of papillary thyroid carcinoma and conventional papillary thyroid carcinoma].

OBJECTIVE: To investigate the expression and clinical significance of Muc1, p63 protein in diffuse sclerosing variant of papillary thyroid carcinoma and conventional papillary thyroid carcinoma. METHOD: Immunohistochemistry (SP) was used to detect the expressions of Muc1, p63 protein in 30 samples of DSVPTC (experiment group) and 30 samples of CPTC (control group). Patients in two groups were matched in age, gender, tumor side, tumor size and date of diagnosis. RESULT: (1) The positive rate of Muc1 in DSVPTC and CPTC was 76.67% (23/30) and 53.33% (16/30) respectively, immunohistochemical staining expressed as brown or tan particles in the membrane or the cytoplasm,with a significant difference between the two groups (P < 0.05). The positive rate of p63 in DSVPTC and CPTC was 80% (24/30) and 43.33% (13/30) respectively, immunohistochemical staining expressed as a brown or tan particles in the muclei,with a significant difference between the two groups (P < 0.05). (2) Cervical lymph node metastasis rate in DSVPTC and CPTC was 50% (15/30) and 20% (6/30) respectively, with a significant difference between the two groups (P < 0.05). (3) In All cases,the positive rate of Muc1 in cervical lymph node metastasis group (21 cases) and without metastasis group (39 cases) was 85.71% (18/21) and 53.85% (21/39) respectively,with a significant difference between the two groups (P < 0.05); the positive rate of p63 was 95.24% (20/21) and 43.59% (17/39) respectively,with a significant difference between the two groups (P < 0.01). (4) Spearman rank correlation analysis showed that expression of Muc1 and p63 were positively correlated in both groups(r = 0.530,0. 386, P < 0.05). CONCLUSION: (1) There are high expression of Muc1 and p63 protein in DSVPTC, and relatively low expression in CPTC, DSVPTC have a higher rate of cervical lymph node metastasis at the time of being diagnosed, compared to the CPTC. These results show that DSVPTC is a more biologically aggressive variant of the PTC. (2) Abnormal expression of Muc1 and p63 may be important to promote the progression and metastasis of PTC, thus they can be used as predictors of malignant behavior in PTC. (3) Muc1 and p63 may be synergistically promote proliferation and invasion metastasis of the PTC malignant cell.

Nanoclusters of gold on a high-area support: almost uniform nanoclusters imaged by scanning transmission electron microscopy.

Highly dispersed supported gold offers unprecedented catalytic properties. Determination of the dependence of the catalytic properties on the gold nanocluster size requires the preparation of size-controlled gold nanoclusters on support surfaces with a high degree of uniformity. Starting from site-isolated mononuclear gold complexes on high-area MgO, we demonstrate the preparation of gold clusters consisting of <10 atoms. These samples have been imaged with atomic resolution by aberration-corrected scanning transmission electron microscopy. The images show that treatment of the supported mononuclear complexes at 318 K in flowing helium caused aggregation of the gold into clusters of 2-6 atoms, present with unconverted individual site-isolated mononuclear gold species and in the absence of any larger nanoparticles. Treatment of the sample at a higher temperature (373 K) in flowing helium resulted in the formation of gold clusters with diameters of 0.58 +/- 0.15 nm (containing roughly 10 Au atoms), again in the absence of larger nanoparticles. Upon exposure of the supported nanoclusters to the electron beam, they underwent aggregation to gold clusters approximately 1 nm in average diameter, as shown in consecutive STEM images.

Oxidation by CO2 of Au0 species on La2O3-supported gold clusters.

The IR spectra that characterize La(2)O(3)-supported gold clusters show that the original Au(0) species can be oxidized by CO(2) during the catalytic CO oxidation reaction, indicating that CO(2) is the actual gold oxidizing agent.

Increasing the number of oxygen vacancies on TiO2 by doping with iron increases the activity of supported gold for CO oxidation.

The addition of iron to high-area TiO2 (Degussa P25, a mixture of anatase and rutile) increases the number of oxygen defect sites that react with O2 to form peroxide and superoxide species. In the presence of gold nanoclusters on the TiO2 surface, the superoxide species become highly reactive, and the activity of the supported gold catalyst for CO oxidation is approximately twice that of the most active comparable catalysts described in the literature. Images of the catalyst obtained by scanning transmission electron microscopy combined with spectra of the catalyst measured in the working state (Raman, extended X-ray absorption fine structure, and X-ray absorption near-edge structure) indicate strong interactions of gold with the support and the presence of iron near the interfaces between the gold clusters and the TiO2 support. The high activity of the catalysts is attributed to the presence of defects in these sites that activate oxygen.

Oxide- and zeolite-supported molecular metal complexes and clusters: physical characterization and determination of structure, bonding, and metal oxidation state.

This article is a review of the physical characterization of well-defined site-isolated molecular metal complexes and metal clusters supported on metal oxides and zeolites. These surface species are of interest primarily as catalysts; as a consequence of their relatively uniform structures, they can be characterized much more precisely than traditional supported catalysts. The properties discussed in this review include metal nuclearity, oxidation state, and ligand environment, as well as metal-support interactions. These properties are determined by complementary techniques, including transmission electron microscopy; X-ray absorption, infrared, Raman, and NMR spectroscopies; and density functional theory. The strengths and limitations of these techniques are assessed in the context of results characterizing samples that have been investigated thoroughly and with multiple techniques. The depth of understanding of well-defined metal complexes and metal clusters on supports is approaching that attainable for molecular analogues in solution. The results provide a foundation for understanding the more complex materials that are typical of industrial catalysts.