Coordination-Modulated Metal Tetrathiafulvalene Octacarboxylate Frameworks for High-Performance Lithium-Ion Battery Anodes.

Modulation of the ligands and coordination environment of metal-organic frameworks (MOFs) has been an effective and relatively unexplored avenue for improving the anode performance of lithium-ion batteries (LIBs). In this study, three MOFs are synthesized, namely, M4 (o-TTFOB)(bpm)2 (H2 O)2 (where M is Mn, Zn, and Cd; o-H8 TTFOB is ortho-tetrathiafulvalene octabenzoate; and bpm is 2,2'-bipyrimidine), based on a new ligand o-H8 TTFOB with two adjacent carboxylates on one phenyl, which allows us to establish the impact of metal coordination on the performance of these MOFs as anode materials in LIBs. Mn-o-TTFOB and Zn-o-TTFOB, with two more uncoordinated oxygen atoms from o-TTFOB8- , show higher reversible specific capacities of 1249 mAh g-1 and 1288 mAh g-1 under 200 mA g-1 after full activation. In contrast, Cd-o-TTFOB shows a reversible capacity of 448 mAh g-1 under the same condition due to the lack of uncoordinated oxygen atoms. Crystal structure analysis, cyclic voltammetry measurements of the half-cell configurations, and density functional theory calculations have been performed to explain the lithium storage mechanism, diffusion kinetics, and structure-function relationship. This study demonstrates the advantages of MOFs with high designability in the fabrication of LIBs.

[Overexpression of miR-382-5p Mediated Downregulation of PTEN on Malignant Biological Behavior of Human Glioma U251 Cells].

OBJECTIVE: To investigate the effect of overexpression of miR-382-5p overexpression on malignant biological behavior of human glioma U251 cells. METHODS: U251 cells were transfected with miR-382-5pmimic. Then miR-382-5p and PTEN mRNA levels were detected by reverse transcription-polymerase chain reaction (RT-PCR) after transfection. Used bioinformatics to predicted the presence of base binding sites between miR-382-5p and PTEN, and constructed PTEN pcDNA vector overexpression plasmid was constructed. Luciluciase reporting experiment was used to detect the targeting relationship between miR-382-5p and PTEN. Cells were randomly divided into four groups: control group, mimics group, pc-PTEN group and mimics+pc-PTEN group for follow-up experiments. RT-PCR was carried out to detect the level of PTEN mRNA in each group. Cell proliferation was detected by clone formation method. The mRNA levels of Ki67, Survivin and c-Myc were detected by RT-PCR. Transwell experiment was used to assayed cell invasion ability. The expression levels of E-cadherin, N-cadherin and Vimentin were determined by Western blot. RESULTS: Results showed that miR-382-5p directly targeted PTEN. Compared with the control group, miR-382-5p and c-Myc mRNA levels and E-cadherin protein level were increased (P<0.05),PTEN, Ki67 and Survivin mRNA levels were decreased (P<0.05), cell clonal formation rate and cell invasion number were decreased (P<0.05), N-cadherin and Vimentin protein levels were decreased (P<0.05) in the mimics group; In pc-PTEN group, miR-382-5p mRNA and c-Myc mRNA levels and E-cadherin protein level were decreased (P<0.05),PTEN, Ki67 and Survivin mRNA levels were increased (P<0.05), cell clonal formation rate and cell invasion number were increased (P<0.05), N-cadherin and Vimentin protein levels were increased (P<0.05). Compared with pc-PTEN group, PTEN, Ki67 and Survivin mRNA levels, the cell clone formation rate, the number of invasion cells and the N-cadherin and Vimentin levels of mimics+PC-PTEN group decreased significantly (P<0.05), while the c-Myc mRNA level and E-cadherin protein level increased significantly (P<0.05). CONCLUSION: Overexpression of miR-382-5p mediates the downregulation of PTEN expression, causing the inhibition of the proliferation, invasion, growth and EMT of U251 glioma cells.

CBX3 promotes glioma U87 cell proliferation and predicts an unfavorable prognosis.

BACKGROUND: Chromobox protein homolog 3 (CBX3) is one of the heterochromatin protein 1 (HP1) family members. Among multiple cancers, it is usually overexpressed. However, the mechanism and function of CBX3 in glioma remain incompletely illustrated. METHODS: The expression level of CBX3 as well as its correlation with glioma are detected through TCGA and Oncomine database. The expressions of CBX3 mRNA and protein in glioma tissues and normal brain tissues have been identified by qRT-PCR and Western blot. The prognostic role of CBX3 has been assessed in a retrospective cohort study. Additionally, the correlation between CBX3 expression and the clinicopathological characteristics of glioma patients were also discussed. To better understand the role of CBX3 in glioma, a lentiviral vector expressing CBX3-shRNA and cyclin dependent kinase inhibitor 1A (CDKN1A) siRNA were established and transfected into the glioma U87 cells. Besides, the CBX3 and CDKN1A expression levels in glioma U87 cells after transfected with CBX3-shRNA were gauged by qRT-PCR and Western blot. CCK-8, colony formation and EdU assays have been applied to evaluate the influence of CBX3 on U87 cells proliferation, and flow cytometry has been applied to manage the changes in cell cycle and cell apoptosis after transfection with CBX3-shRNA. Xenograft tumors have been examined in vivo for the carcinogenic effects and prognostic value of CBX3 in glioma tissues. RESULTS: In the present study, CBX3 was demonstrated to be highly expressed in human glioma tissues, and high CBX3 expression predicted the dismal recurrence-free survival (RFS) and poor overall survival (OS) for glioma patients. High CBX3 expression was dependent on the tumor size, Karnofsky performance scale (KPS) score, WHO grade, recurrence and survival status. Moreover, CBX3 expression knockdown could remarkably suppress the proliferation and colony formation ability of U87 cells, which was achieved through blocking cell arrest at G0/G1 phase and inducing apoptosis. Additionally, our findings also suggested that, compared with shRNA-Ctrl transfection, the mRNA and protein expression levels of CDKN1A have been dramatically up-regulated in vitro after transfection with shRNA-CBX3. Consistent with the results of in vitro assays, the outcomes of xenograft assay and immunohistochemistry (IHC) also indicated that, the tumor growth and Ki-67 expression level were restrained in response to CBX3 inhibition, while the CDKN1A expression level in vivo was up-regulated. Down-regulation of CDKN1A expression partially restored the ability of cell proliferation in the U87 cells, which was inhibited by shRNA-CBX3 CONCLUSIONS: In conclusion, results of the current research suggest that a high CBX3 expression level predicts the poor prognosis for glioma patients. CBX3 can stimulate the growth of glioma U87 cells through targeting CDKN1A and CBX3 may become a novel target in the clinical treatment for glioma.

Cell division cycle associated 7 like predicts unfavorable prognosis and promotes invasion in glioma.

BACKGROUND: Cell division cycle associated 7 like (CDCA7L) belongs to the JPO protein family, which is recently identified as a target gene of c-Myc and is frequently dysregulated in multiple cancers. This study aimed to explore the clinicpathological value and biological role of CDCA7L in glioma. METHODS: CDCA7L expression in glioma patients was determined using the Oncomine database, and the prognostic role of CDCA7L expression was assessed in a retrospective cohort study. Moreover, the relationship of CDCA7L expression with the clinicopathological characteristics in glioma patients, including age, gender, tumor size, cystic change, Karnofsky performance scale (KPS) score, tumor location, extent of resection, WHO grade, adjuvant therapy and tumor recurrence, was analyzed in this study. In addition, the CDCA7L small interfering (si) RNA was constructed and transfected into the glioma U251 cells, so as to examine the role of CDCA7L in glioma patients. Besides, the changes in U251 cell invasion after transfection with CDCA7L siRNA were also monitored through Transwell assay. RESULTS: Our results suggested that CDCA7L expression was up-regulated in different glioma types, including glioblastoma, oligodendroglioma, diffuse astrocytoma and anaplastic astrocytoma. Moreover, the current retrospective cohort study indicated that high CDCA7L expression was associated with tumor size, WHO grade, adjuvant therapy and recurrence, as well as the poor overall survival (OS) and recurrence-free survival (RFS) in glioma patients. Lastly, CDCA7L expression was knocked down using CDCA7L siRNA, which could block the invasion abilities of glioma U251 cells. CONCLUSIONS: CDCA7L is highly expressed in human glioma tissues and a high CDCA7L expression level predicts the dismal prognosis for glioma patients. Moreover, CDCA7L can promote glioma invasion, which can serve as an independent potential prognostic biomarker for glioma patients.

The nucleocytoplasmic translocation and up-regulation of ING5 protein in breast cancer: a potential target for gene therapy.

Here, we found that ING5 overexpression resulted in a lower proliferation, reduced glucose metabolism, S arrest, decreased migration and invasion, apoptotic induction, fat accumulation, autophagy, senescence and mesenchymal-epithelial-transition of breast cancer cells. It also suppressed the tumor growth of breast cancer cells by inhibiting proliferation, inducing apoptosis and autophagy. ING5-mediated chemoresistance was positively linked to Akt and NF-κB activation, MRP1 and GST-π overexpression, and FBXW7 hypoexpression. ING5 expression was higher in breast cancer than normal tissue at both mRNA and protein levels. ING5 mRNA expression was positively correlated with relapse- and distant metastasis-free survival rates. Nuclear ING5 expression showed gradual decrease from breast normal tissue, fibroadenoma, adenomatosis, primary to metastatic cancers, while versa for cytoplasmic ING5. Nuclear ING5 expression was negatively correlated with distant metastasis and p53 hypoexpression, while cytoplasmic ING5 expression was positively correlated with tumor size and ER expression. These data suggested that up-regulated expression and nucleocytoplasmic translocation of ING5 protein were observed in breast cancer. The higher expression of nuclear ING5 was inversely linked to worse clinicopathological behaviors of breast cancer by in vivo and vitro reversing aggressive phenotypes. Therefore, it should be employed as a biomarker to indicate the tumorigenesis and aggressiveness of breast cancer, and as a potential target for gene therapy.

Identification of proteins associated with lymph node metastasis of gastric cancer.

PURPOSE: The aim of this study was to identify proteins associated with gastric cancer lymph node metastasis and explore the clinicopathological significance of these proteins. METHODS: Gastric cancer tissues were obtained from 24 patients with high or low lymph node metastatic potential. Total cellular proteins were separated by two-dimensional gel electrophoresis (2-DE), analyzed by MALDI/TOF-TOF MS, and identified by a database search. Expression of 14-3-3ß and profilin-1 was then immunohistochemically verified in paraffin-embedded gastric cancer tissues from 128 patients and analyzed by multivariate logistic regression models, Kaplan-Meier curves, and Cox proportional hazard models. RESULTS: A total of 26 differentially expressed proteins were identified, 20 of which were overexpressed and 6 of which were underexpressed. 14-3-3ß and profilin-1 were upregulated in gastric cancer tissues with and without lymph node metastasis, respectively. Expression of 14-3-3ß protein was associated, but profilin-1 expression was inversely associated with gastric cancer lymph node metastasis. Multivariate analysis showed that overexpression of 14-3-3ß and reduced expression of profilin-1 were independent risk factors for gastric cancer lymph node metastasis, while 14-3-3ß overexpression was an independent prognostic factor for gastric cancer patients. CONCLUSIONS: The current study identified 26 differentially expressed proteins. Further studies showed that both 14-3-3ß and profilin-1 protein may be useful biomarkers for prediction of gastric cancer lymph node metastasis and that expression of 14-3-3ß was a prognostic marker for gastric cancer patients.

Expression of tissue levels of matrix metalloproteinases and tissue inhibitors of metalloproteinases in gastric adenocarcinoma.

BACKGROUND AND OBJECTIVES: Matrix metalloproteinases (MMPs) are one of the major classes of proteolytic enzymes involved in tumor invasion and metastasis, being inhibited by naturally occurring tissue inhibitors of metalloproteinases (TIMPs). We examined mRNA expression for MMP-2, MMP-7, MMP-9, MT1-MMP, TIMP-1, and TIMP-2 in human gastric adenocarcinoma tissues, and the correlation between their expression and clinicopathological variables. METHODS: Gastric tissue samples from 72 patients with gastric adenocarcinoma were available for this study. To determine mRNA expression for MMP-2, MMP-7, MMP-9, MT1-MMP, TIMP-1, and TIMP-2, semiquantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was carried out on tumor and normal tissues, respectively. RESULTS: Mean MMP-2, MMP-7, MMP-9, MT1-MMP, TIMP-1, and TIMP-2 mRNA expression in the gastric adenocarcinomas was significantly higher than in the normal tissue. In terms of the invasion of the tumor, lymph node metastasis, and tumor stage of gastric adenocarcinoma, the differences in MMP-2, MMP-7, MMP-9, and MT1-MMP mRNA expression levels were significant. MMP-2, MMP-7, MMP-9, MT1-MMP, TIMP-1, and TIMP-2 mRNA expression did not differ significantly in relation to histological type of gastric adenocarcinoma. CONCLUSION: The correlation between the increased expression of MMP-2, MMP-7, MMP-9, and MTI-MMP and clinicopathological parameters reflects a role in predicting the aggressive behavior of gastric cancer.