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Drug resistance is often developed during clinical chemotherapy of ovarian cancers. The ubiquitin‐like protein interferon‐stimulated gene 15 (ISG15) is possibly dependent on tumour context to promote or suppress progression of various tumours. The ubiquitin‐like protein interferon‐stimulated gene 15 (ISG15) was decreased in cisplatin‐resistant ovarian cancer cells. The current study identified that both ectopic wild type and nonISGylatable mutant ISG15 expression inhibited CSC‐like phenotypes of cisplatin‐resistant ovarian cancer cells. Moreover, ectopic ISG15 expression suppressed tumour formation in nude mice. In addition, ISG15 downregulation promoted CSC‐like features of cisplatin‐sensitive ovarian cancer cells. Furthermore, low ISG15 expression was associated with poor prognosis in patients with ovarian cancer. Transcriptional repressor Krüppel‐like factor 12 (KLF12) downregulated ISG15 in cisplatin‐resistant cells. Our data indicated that downregulating ISG15 expression, via weakening effect of KLF12, might be considered as new therapeutic strategy to inhibit CSC phenotypes in the treatment of cisplatin‐resistant ovarian cancer.

An imidazolium-based ionic liquid (IL) was employed and modified by sodium lignosulfonate (LnNa) to synthesize hierarchical ETS-10 zeolite with porous structure, morphology and surface properties effectively adjusted. The template and structure-directing effects of both IL and LnNa proved to be well maintained after modification. And more importantly, the unique molecular recognition of LnNa was preserved well, while the aggressiveness of LnNa implementing through interaction with other inorganic species can be efficiently suppressed. This led to the formation of hierarchical ETS-10 zeolite with not only high crystallinity and structure integrity but also enhanced catalytic performance in aqueous-phase biomass conversion. Thus, for guaiacol hydrodeoxygenation, a notable conversion (92.8%) and cyclohexane yield (89.7%) can be acquired. This remarkable catalytic reactivity should be owing to its distinguished analogous molecular recognition pattern, promoted crystallinity, modified morphology and porous structure, and what’s more, the strengthened acid property.

Solid tumour frequently undergoes metabolic stress during tumour development because of inadequate blood supply and the high nutrient expenditure. p53 is activated by glucose limitation and maintains cell survival via triggering metabolic checkpoint. However, the exact downstream contributors are not completely identified. BAG3 is a cochaperone with multiple cellular functions and is implicated in metabolic reprogramming of pancreatic cancer cells. The current study demonstrated that glucose limitation transcriptionally suppressed BAG3 expression in a p53‐dependent manner. Importantly, hinderance of its down‐regulation compromised cellular adaptation to metabolic stress triggered by glucose insufficiency, supporting that BAG3 might be one of p53 downstream contributors for cellular adaptation to metabolic stress. Our data showed that ectopic BAG3 expression suppressed p53 accumulation via direct interaction under metabolic stress. Thereby, the current study highlights the significance of p53‐mediated BAG3 suppression in cellular adaptation to metabolic stress via facilitating p53 accumulation.

As an environment-friendly natural gas hydrate exploitation method, CO2 replacement method can not only achieve the purpose of mining natural gas hydrate, but also store the current greenhouse gas CO2 in the form of hydrate on the seabed, and maintain the stratum stability of hydrate deposit area. In order to improve the rate and efficiency of CH4-CO2 replacement reaction, researchers proposed to use CO2 contained gas mixture instead of pure CO2 to replace CH4 in natural gas hydrate. Based our previous work about CH4 hydrate recovery with 40% CO2 + 60% H2, in this study, the effect of gas concentration in gas phase on final CH4 recovery are investigated by implying different time interval of gas exchange operation. Experimental results show that The CH4 recovery efficiency is 10.41 when the gas exchange is continues through the whole replacement process, and CH4 recovery efficiency changes to 12.25, 32.24 and 28.86 when gas exchange operation is carried out every 12, 24, 36 h. Indicating that replaced CH4 needs to be discharged in time to avoid CH4 molecules being replaced to form hydrates again, and it is necessary to accurately control the time interval of gas exchange operation to avoid insufficient contact time between CO2 and H2 molecules and CH4 hydrate, which affects the final replacement efficiency. In addition, the mechanism of CO2 gas mixture containing small gas molecule such as H2, N2 are studied. The results indicate that when CO2 containing small molecules such as H2 and N2 displace CH4 hydrate, the existence of small molecules (H2, N2) can give rise to decompose the hydrate lattice and release CH4 gas. If the gas molecules (CO2, N2, H2, CH4) in the gas phase have enough driving force to enter the hydrate lattice and remain stability, CH4 hydrate will not decompose completely; If not, CH4 hydrate will be completely decomposed.

Ovarian cancer (OC) is a common gynecological malignant tumor that seriously endangers the health of women worldwide. Tripartite motif containing 29 (TRIM29) is a TRIM family member that is frequently overexpressed in OC. However, the specific role of TRIM29 in OC remains obscure. To investigate the underlying molecular mechanism, a global proteomics analysis identified SET binding protein 1 (SETBP1) as a crucial target of TRIM29. Subsequently, the SETBP1/SET/Protein phosphatase 2 (PP2A) axis was confirmed to be required for the recovery of cancer stem cell (CSC)-like phenotype suppressed by TRIM29 knockdown. Mechanistically, TRIM29 facilitated SETBP1 transcriptional activation via the VEZF1 transcription factor. More importantly, TRIM29 promoted VEZF1 mRNA translation by recruiting RNA binding protein BICC1 to its 3'UTR. The clinical significance was established by the association of TRIM29 and SETBP1 expression with clinicopathological features in OC samples. The SETBP1/SET/PP2A axis driven by TRIM29 via transcription factor VEZF1 is at least one of the primary mechanisms underlying TRIM29 maintenance of the CSC-like characteristics in OC.

Glucose limitation activates p53, which functions as an adaptive response to maintain cell survival. However, p53 is frequently deleted or mutated in a variety of tumors, while most cancer cells can acclimatize themselves to metabolically unfavorable surrounding, indicating that alternative mechanisms other than p53 transactivation underly adaptive response of cancer cells with p53 deletion or mutation to metabolically hostile environment. Sestrin 2 (SESN2) is a p53 downstream target, which plays a protective role against various stressful stimuli, such as genotoxic, energetic, and oxidative stress. In the current study, we demonstrated that SESN2 transcript was stabilized by glucose limitation at the posttranscriptional level irrespective of p53 status. Importantly, SESN2 also protected cells from metabolic stress triggered by glucose limitation in a p53-independent manner. Our data indicated that stabilization of SESN2 transcript might be an alternative adaptive response to metabolic stress other than p53 activation. Thereby, the current study highlights the significance of stabilization of SESN2 transcript in adaptation of cells with p53 deletion or mutation to metabolic stress.

BAG3 is constitutively expressed in multiple types of cancer cells and its high expression is associated with tumour progression and poor prognosis of PDAC. However, little is known about the role of BAG3 in the regulation of stromal microenvironment of PDAC. The current study demonstrated that beside PDAC tumour cells, BAG3 was also expressed in some activated stroma cells in PDAC tissue, as well as in activated PSCs. In addition, the current study demonstrated that BAG3 expression in PSCs was involved in maintenance of PSCs activation and promotion of PDACs invasion via releasing multiple cytokines. The current study demonstrated that BAG3‐positive PSCs promoted invasion of PDACs via IL‐8, MCP1, TGF‐β2 and IGFBP2 in a paracrine manner. Furthermore, BAG3 sustained PSCs activation through IL‐6, TGF‐β2 and IGFBP2 in an autocrine manner. Thereby, the current study provides a new insight into the involvement of BAG3 in remodelling of stromal microenvironment favourable for malignant progression of PDAC, indicating that BAG3 might serve as a potential target for anti‐fibrosis of PDAC.

Bcl-2 associated athanogene 3 (BAG3) is an important molecule that maintains oncogenic features of cancer cells via diverse mechanisms. One of the important functions assigned to BAG3 is implicated in selective macroautophagy/autophagy, which attracts much attention recently. However, the mechanism underlying regulation of autophagy by BAG3 has not been well defined. Here, we describe that BAG3 enhances autophagy via promotion of glutamine consumption and glutaminolysis. Glutaminolysis initiates with deamination of glutamine by glutaminase (GLS), by which yields glutamate and ammonia in mitochondria. The current study demonstrates that BAG3 stabilizes GLS via prohibition its interaction with SIRT5, thereby hindering its desuccinylation at Lys158 and Lys164 sites. As an underlying molecular mechanism, we demonstrate that BAG3 interacts with GLS and decreases SIRT5 expression. The current study also demonstrates that occupation by succinyl at Lys158 and Lys164 sites prohibits its Lys48-linked ubiquitination, thereby preventing its subsequent proteasomal degradation. Collectively, the current study demonstrates that BAG3 enhances autophagy via stabilizing GLS and promoting glutaminolysis. For the first time, this study reports that succinylation competes with ubiquitination to regulate proteasomal GLS degradation.

Ovarian cancer is the most lethal gynecologic malignant cancer, frequently due to its late diagnosis and high recurrence. Cancer stem cells (CSCs) from different malignancies including ovarian cancer have been linked to chemotherapy resistance and poor prognosis. Therefore, identifying the molecular mechanisms mediating therapy resistance is urgent to finding novel targets for therapy-resistant tumors. Aberrant O-glycosylation ascribed to subtle alteration of GALNT family members during malignant transformation facilitate metastasis in various cancers. The current study demonstrated that BAG3 was upregulated in platin-resistant ovarian cancer tissues and cells, and high BAG3 predicted dismal disease-free survival of patients with ovarian cancer. In addition, the current study showed that BAG3 facilitated CSC-like properties of ovarian cancer cells via regulation of GALTN10. In a term of mechanism, BAG3 epigenetically regulated GALNT10 transactivation via histone H3 lysine 4 (H3K4) presenter WDR5. We demonstrated that WDR5 increased H3K4 trimethylation (H3K4me3) modification at the promoter regions of GALNT10, facilitating recruitment of transcription factor ZBTB2 to the GALNT10 promoter. Collectively, our study uncovers an epigenetic upregulation of GALNT10 by BAG3 via WDR5 to facilitate CSCs of platin-resistant ovarian cancers, providing additional information for further identification of attractive targets with therapeutic significance in platin-resistant ovarian cancer.

TRIM29 is dysregulated in pancreatic cancer and implicated in maintenance of stem-cell-like characters of pancreatic cancer cells. However, the exact mechanisms underlying oncogenic function of TRIM29 in pancreatic cancer cells remain largely unclarified. Using a global screening procedure, the current study found that adenylate kinase 4 (AK4) was profoundly reduced by TRIM29 knockdown. In addition, our data demonstrated that TRIM29 knockdown altered bioenergetics and suppressed proliferation and invasion of pancreatic cancer cells via downregulation of AK4 at the posttranscriptional level. The current study demonstrated that upregulation of microRNA-2355-3p (miR-2355-3p) upregulated AK4 expression via facilitating DDX3X recruitment to the AK4 transcript, and TRIM29 knockdown thereby destabilized the AK4 transcript via miR-2355-3p downregulation. Collectively, our study uncovers posttranscriptional stabilization of the AK4 transcript by miR-2355-3p interaction to facilitate DDX3X recruitment. Regulation of AK4 by TRIM29 via miR-2355-3p thereby provides additional information for further identification of attractive targets for therapy with pancreatic cancer., Graphical Abstract, Hao et al. reported that TRIM29 altered biogenergetics via posttranscriptional regulation of AK4 in PDACs. In mechanism, TRIM29 knockdown suppressed miR-2355-3p expression and subsequently reduced recruitment of DDX3X to 3′ UTR of the AK4 transcript. The TRIM29/miR-2355-3p/DDX3X/AK4 pathway may provide information for further identification of attractive targets for therapy in pancreatic cancer.

With the demand of energy and re-utilization of wastes, the renewable lignocellulosic biomass, has attracted increasing and significant attention for alleviating the growing energy crisis and environment problems. As main components of lignocellulosic biomass, lignin, cellulose, and hemicellulose are connected by hydrogen bond to form a compact skeleton structure, resulting the trenchant condition of biomass pyrolysis. Also, pyrolysis products of above three main constituents contain a large amount of oxygenates that cause low heating value, high corrosiveness, high viscosity, and instability. Meanwhile, zeolites are of considerable significance to the conversion of lignocellulosic biomass to desirable chemical products on account of fine shape selectivity and moderate acid sites and strength. Among numerous zeolites, ZSM-5-based catalysts have been most extensively studied, and the acidity and porosity of ZSM-5 can be tuned by changing the content of Si or Al in zeolite. Beyond that, doping of other metal elements, such as Mn, Co, Ni, Ga, Ce, Pt, into ZSM-5 is also an efficient way to regulate the strength and density of acid sites in zeolite precisely. This review focused on the recent investigation of Ni-modified microporous ZSM-5 used in catalytic pyrolysis of lignin and cellulose. The application of metal-modified hierarchical ZSM-5 is also covered.

Cancer cells frequently exhibit aerobic glycolysis, known as the Warburg effect. An et al. identify a novel RNA regulatory activity of BAG3, a protein implicated in various cancers. BAG3 enhances posttranscriptionally the expression of Hexokinase 2, the first enzyme involved in glycolysis, and it reprograms glucose metabolism by pancreatic cancer cells., Aerobic glycolysis, a phenomenon known historically as the Warburg effect, is one of the hallmarks of cancer cells. In this study, we characterized the role of BAG3 in aerobic glycolysis of pancreatic ductal adenocarcinoma (PDAC) and its molecular mechanisms. Our data show that aberrant expression of BAG3 significantly contributes to the reprogramming of glucose metabolism in PDAC cells. Mechanistically, BAG3 increased Hexokinase 2 (HK2) expression, the first key enzyme involved in glycolysis, at the posttranscriptional level. BAG3 interacted with HK2 mRNA, and the degree of BAG3 expression altered recruitment of the RNA-binding proteins Roquin and IMP3 to the HK2 mRNA. BAG3 knockdown destabilized HK2 mRNA via promotion of Roquin recruitment, whereas BAG3 overexpression stabilized HK2 mRNA via promotion of IMP3 recruitment. Collectively, our results show that BAG3 promotes reprogramming of glucose metabolism via interaction with HK2 mRNA in PDAC cells, suggesting that BAG3 may be a potential target in the aerobic glycolysis pathway for developing novel anticancer agents.

Ovarian cancer is the most frequent cause of gynecologic malignancies associated death. Primary or acquired cisplatin resistance is frequently occurred during ovarian cancer therapy. Cancer stem cells (CSC) tend to form minimal residual disease after chemotherapy and are implicated in relapse. The ability of cancer cells to reprogram their metabolism has recently been related with maintenance of CSC and resistance to chemotherapies. The current study found that BAG5 expression was decreased in cisplatin-resistant ovarian cancer cells and clinical tissues. Our data demonstrated that BAG5 knockdown was implicated in metabolic reprogramming and maintenance of cancer stem cell (CSC)-like features of ovarian cancer cells via regulation of Rictor and subsequent mTORC2 signaling pathway. In addition, the current study demonstrated that Bcl6 upregulation was responsible for repression of BAG5 transactivation via recruitment on the BAG5 promoter in cisplatin-resistant ovarian cancer. The current study also demonstrated reverse correlations between BAG5 and Bcl6, BAG5 and Rictor in ovarian serous adenocarcinoma tissues. Collectively, the current study identified the implication of Bcl6/BAG5/Rictor-mTORC2 signaling pathway in metabolic reprograming and maintenance of CSC-like features in cisplatin-resistant ovarian cancer cells. Therefore, further studies on the mechanism underlying regulation of metabolic reprogramming and CSC-like characteristics of cisplatin-resistant ovarian cancer cells may contribute to the establishment of novel therapeutic strategy for cisplatin-resistance.

TRIM family proteins are defined as E3 ubiquitin ligases because of their RING-finger domains. The ubiquitin-like protein interferon-stimulated gene 15 (ISG15) encodes a 15-kDa protein, that is implicated in the posttranslational modification of diverse proteins. Both TRIM29 and ISG15 play both pro-tumoral and anti-tumoral functions in cancer cells derived from different histology. In the current study, we demonstrated that correlation expression of TRIM29 and ISG15 in pancreatic ductal adenocarcinomas (PDACs). The current study demonstrated that TRIM29 knockdown destabilized ISG15 protein via promoting its processing by calpain 3 (CAPN3). Importantly, the current study found that TRIM29 knockdown suppressed cancer stem cell-like features of PDACs, which can be rescued by ISG15 independent of its conjugation function. In addition, the current study demonstrated that extracellular free ISG15 played an important role in maintenance of cancer stem cell-like features of PDACs. Thereby, the current study displayed a novel mechanism by which TRIM29 modulates ISG15 stability via CAPN3-mediated processing, and subsequently extracellular ISG15 maintains the cancer stem cell-like features of PDAC via autocrine mode of action.

Beclin 1 has emerged as a haploinsufficient tumor suppression gene in a variety of human carcinomas. In order to clarify the role of Beclin 1 in thyroid cancer, Beclin 1 was knockdown in thyroid cancer cell lines. The current study demonstrated that knockdown of Beclin 1 resulted in morphological and molecular changes of thyroid cancer cells consistent with epithelial-mesenchymal transition (EMT), a morphogenetic procedure during which cells lose their epithelial characteristics and acquire mesenchymal properties concomitantly with gene expression reprogramming. In addition, the current study presented evidence demonstrating that Beclin 1 knockdown triggered this prometastatic process via stabilization of the EMT inducer ZEB1 mRNA through upregulation of AU-binding factor 1 (AUF1), which is recruited to the 3'-untranslated region (UTR) of the ZEB1 mRNA and decreases its degradation. We also found a negative correlation of Beclin 1 with AUF1 or ZEB1 in thyroid cancer tissues. These results indicated that at least some tumor suppressor functions of Beclin 1 were mediated through posttranscriptional regulation of ZEB1 via AUF1 in thyroid cancers.

Knowledge of the influence of ions of various nature on intermolecular hydrophilic and hydrophobic interactions in solutions is required in many research fields. In this paper, dilution enthalpies of zwitterion l -carnitine in aqueous NaCl, KCl and NaBr solutions of various molalities (b = 0 to 3.0 mol · kg−1) have been determined respectively at T = (298.15 ± 0.01) K and p = (0.100 ± 0.005) MPa by isothermal titration calorimetry (ITC). In light of the MacMillan–Mayer theory, the 2nd virial enthalpic coefficients (h2) have been calculated. The h2 coefficients increase gradually with increasing molality (b) of the three aqueous alkali halides solutions, from small negative values in pure water to relatively larger positive values in solution. The trends of h2 coefficients are ascribed to the salt effects on the balance between hydrophilic and hydrophobic interactions in pairwise self-associations. It is considered that the size of cations and anions exert influences on h2 coefficients through their surface charge densities and hydration (or dehydration) abilities.

Dilution enthalpies of urea (U) and its four derivatives {biuret (BU), methylurea (MU), 1,1-dimethylurea (1,1-DMU) and 1,3-dimethylurea (1,3-DMU)} in (dimethylformamide (DMF) + water) mixtures of various mole fractions ( x DMF = 0 to 0.10) at T = 298.15 K have been determined by isothermal titration calorimetry (ITC). In light of the approach of McMillan–Mayer’s theory, enthalpic pairwise self-interaction coefficients ( h 2 ) of each compound at the corresponding composition ( x DMF ) of mixed solvent (DMF + water) have been calculated. It is found that the h 2 coefficients of each compound are all negative in pure water and increase incrementally with the concentration of DMF in the mixed solvent, following the order h 2 (BU) h 2 (U) h 2 (MU) h 2 (1,1-DMU) h 2 (1,3-DMU). It is concluded that (1) the addition of co-solvent DMF to solvent water is unfavourable to the pairwise self-interactions of these solutes from the point of view of enthalpy; (2) the substitution of methyl (Me) on N atom of urea enhances the component of hydrophobic interactions during the pairwise self-interactions of these solutes; (3) BU is a more hydrophilic molecule than U, and 1,3-DMU is a more hydrophobic molecule than 1,1-DMU.

// De-Hui Kong 1, 2 , Si Li 1 , Zhen-Xian Du 3 , Chuan Liu 4 , Bao-Qin Liu 1 , Chao Li 1 , Zhi-Hong Zong 1 , Hua-Qin Wang 1, 2 1 Department of Biochemistry and Molecular Biology, China Medical University, Shenyang, China 2 Key Laboratory of Cell Biology, Ministry of Public Health, and Key Laboratory of Medical Cell Biology, Ministry of Education, China Medical University, Shenyang, China 3 Department of Endocrinology and Metabolism, The 1st Affiliated Hospital, China Medical University, Shenyang, China 4 Department of Gynecology and Obstetrics, Shengjing Hospital, China Medical University, Shenyang, China Correspondence to: Hua-Qin Wang, e-mail: wanghq_doctor@hotmail.com Keywords: BAG3, HCCs, G6PD, pentose phosphate pathway Received: April 26, 2015 Accepted: November 14, 2015 Published: November 26, 2015 ABSTRACT Bcl-2 associated athanogene 3 (BAG3) contains multiple protein-binding motifs to mediate potential interactions with chaperons and/or other proteins, which is possibly ascribed to the multifaceted functions assigned to BAG3. The current study demonstrated that BAG3 directly interacted with glucose 6 phosphate dehydrogenase (G6PD), the rate-limiting enzyme of the pentose phosphate pathway (PPP). BAG3 suppressed the PPP flux, de novo DNA synthesis and cell growth in hepatocellular carcinomas (HCCs). The growth defect of HCCs with forced BAG3 expression can be rescued by enforced G6PD expression. However, BAG3 elevation did not cause a reduction in cellular NADPH concentrations, another main product of G6PD. In addition, supplement of nucleosides alone was sufficient to recover the growth defect mediated by BAG3 elevation. Collectively, the current study established a tumor suppressor-like function of BAG3 via direct interaction with G6PD in HCCs at the cellular level.

The dilution enthalpies of four derivatives of monosaccharides, namely 2-deoxy- d -glucose (2-DGlu), N-acetyl- d -glucosamine (GluNAc), 2-deoxy- d -galactose (2-DGal) and N-acetyl- d -galactosamine (GalNAc), in aqueous NaCl solutions of various molalities (b = 0–3.0 mol · kg−1) have been determined respectively at T = 298.15 K by isothermal titration calorimetry (MicroCal ITC200). The corresponding values of enthalpic pairwise self-interaction coefficients (h2) have been calculated according to the McMillan–Mayer theory. It was found that across the range studied of ionic strength (I) or molality (b = I), the h2 coefficients are all positive, in the order h2 (GluNAc) > h2 (GalNAc) > h2 (2-DGlu) > h2 (2-DGal), and decrease gradually after increasing first up to a maximum at b ≈ 1.5 mol · kg−1. The effects of ionic strength (I) on the trends of h2 have been discussed from the point of view of complex (solute + solute) and (solute + solvent) interactions in solutions.

Papillary thyroid cancer (PTC), the most common thyroid malignancy, has a strong propensity for neck lymph node metastasis, which will increase the risk of local recurrence and decrease the survival in some high-risk groups. Hence, it is essential to set up a reliable biomarker to predict lymph node metastasis. BAG5 is a unique member of the BAG cochaperone family because it consists of more than one BAG domain, which acts as modulator of chaperone activity. In this study, we found that expression of BAG5 was significantly increased in PTC cells and tissues. Neither overexpression nor downregulation of BAG5 altered the proliferation of PTC cells. On the contrary, overexpression of BAG5 significantly promoted, while knockdown of BAG5 significantly decreased migration and invasion of PTC cells. Along with this, fibronectin 1 (FN1) was significantly increased and decreased in cells that overexpress or downregulate BAG5, respectively. Mechanistically, we found that BAG5 modulated FN1 expression at the translational level and promoted invasion via suppression of miR-144-3p, which targeted the 3' untranslational region (UTR) of FN1 transcript. This study suggests that BAG5 is an important regulator of migration and invasion in PTC cells and may represent a novel therapeutic target for intervening in PTC progression.

Cisplatin-based chemotherapies have long been considered as a standard chemotherapy in ovarian cancer. However, cisplatin resistance restricts beneficial therapy for patients with ovarian cancer. The ubiquitin-like protein interferon-stimulated gene 15 (ISG15) encodes a 15-kDa protein, that is implicated in the post-translational modification of diverse proteins. In this work, we found that ISG15 was downregulated in cisplatin resistant tissues and cell lines of ovarian cancer. Functional studies demonstrated that overexpression of wild type (WT) ISG15, but not nonISGylatable (Mut) ISG15 increased cell responses to cisplatin in resistant ovarian cancer cells. Furthermore, we found that WT ISG15 decreased ABCC2 expression at the protein level. Importantly, overexpression of ABCC2 blocked sensitizing effect of ISG15 on cisplatin. In addition, we identified that hnRNPA2B1 was recruited to 5'UTR of ABCC2 mRNA and promoted its translation, which was blocked by ISG15. We further demonstrated that hnRNPA2B1 could be ISGylated, and ISGylation blocked its recruitment to ABCC2 mRNA, thereby suppressed translation of ABCC2. Altogether, our data support targeting ISG15 might be a potential therapeutic strategy for patients with cisplatin-resistant ovarian cancer.

To investigate the influence of CO2 partial pressure on efficiency of CH4-CO2 swap from natural gas hydrates (NGHs), the replacement of CH4 from natural gas hydrate (NGH) is carried out with simulated Integrated Gasification Combined Cycle (IGCC) syngas under different pressures, and the gas chromatography (GC), in-situ Raman, and powder X-ray diffraction (PXRD) are employed to analyze the hydrate compositions and hydrate structures. The results show that with the P-T (pressure and temperature) condition shifting from that above the hydrate equilibrium curve of IGCC syngas to that below the hydrate equilibrium curve of IGCC syngas, the rate of CH4 recovery drastically rises from 32% to 71%. The presence of water can be clearly observed when P-T condition is above the hydrate equilibrium curve of IGCC syngas; however the presence of water only occurs at the interface between gas phase and hydrate phase. No H2 is found to present in the final hydrate phase at the end of process of CH4-CO2 swap with IGCC syngas.

TS-1 zeolite has outstanding performance in the catalytic reactions with hydrogen peroxide as catalytic promoter. However, the narrow pore size (< 1.0 nm) of traditional TS-1 makes it difficult for bulky organic compounds to contact with the active sites in the pores, which seriously limits application of TS-1. Recently, the introduction of mesoporous structure into microporous TS-1 becomes a hot research topic. Meanwhile, the huge synthesis cost of TS-1 is another main reason hindering its industrial application. In this paper, mesoporous TS-1 was successfully synthesized using sodium silicate as silicon source and titanium trichloride as titanium source under the template conditions of tetrapropylammonium hydroxide (TPAOH) and cationic polymer. The mesoporous TS-1 was characterized by X-ray diffraction (XRD), N2 adsorption, scanning electric microscopy (SEM), transmitting electric microscopy (TEM), Fourier transform infrared spectroscopy (FT-IR) and UV-Vis Spectrum spectra (UV-Vis). Results show that the synthesized TS-1 zeolites have good crystallinity and tetra-coordinated framework Ti atoms, and there are abundant mesoporous structures in the zeolite crystals. The results of oxidation experiments show that conversion of diphenyl sulfide and dibenzyl sulfide with mesoporous TS-1 are 97.3 % and 85.3 % respectively, while that conversion with microporous TS-1 are 75.7 % and 63.5 respectively.

BAG3 is a member of the cochaperone BAG family and often highly expressed in various cancers. Recently, evidences show that BAG3 promotes stemness of human cancer cells. IFN-stimulated genes 15 (ISG15) is an ubiquitin-like molecule, which is covalently conjugated with substrates to form ISGylated proteins. Global screening BAG3 interacting partners demonstrated that ISG15 might be a potential binding partner. The current study revealed that BAG3 did not interact with ISG15, but positively regulated ISG15 expression in pancreatic ductal adenocarcinoma cancer (PDAC). It was further found that BAG3 deletion stabilized ISG15 mRNAs, while suppressed its translation via increasing Serine phosphorylation of Ago2 at position 387 (S387). Both BAG3 deletion and ISG15 knockdown suppressed stem cell-like phenotypes of PDAC cells, including clonogenicity, invasiveness and spheroid formation. In addition, ectopic ISG15 expression rescued the suppressive role of BAG3 deletion in cancer stem cell (CSC)-like phenotypes of PDAC cells, and this effect of ISG15 was independent of its ISGylation function. The current study implies that BAG3 and ISG15 may provide a therapeutic advantage for PDAC.

Bcl-2 associated athanogene 3 (BAG3) is highly expressed in pancreatic ductal adenocarcinoma (PDAC), and its high expression appears to be a poor prognostic factor for patients with PDAC. In this study, we show that BAG3 knockdown significantly decreases migration and invasion of PDACs via reduction of interleukine-8 (IL-8) production. BAG3 knockdown regulates IL-8 expression at the posttranscriptional levels via interplay between recruitment of RNA-binding protein HuR and miR-4312. HuR binds to the cis-elements located in the 3′-untranslational region (UTR) of the IL-8 transcript to stabilize it, whereas miR-4312-containing miRNA-induced silencing complex (miRISC) is recruited to the adjacent seed element to destabilize it. The binding of HuR prevents the recruitment of Argonaute (Ago2), overriding miR-4312-mediated translation inhibition of IL-8. BAG3 knockdown decreases cytoplasmic distribution of HuR via increasing its phosphorylation at Ser202, therefore compromising its recruitment while promoting recruitment of miR-4312 containing miRISC to IL-8 transcript. Furthermore, our data indicate that only phosphorylated Ago2 at Ser387 interacts with IL-8 transcript. BAG3 knockdown increases phosphorylation of Ago2 at Ser387, thereby further promoting loading of miR-4312 containing miRISC to IL-8 transcript. Taken together, we propose that BAG3 promotes invasion by stabilizing IL-8 transcript via HuR recruitment, and subsequently suppressing the loading of miR-4312 containing miRISC in PDACs. Our results reveal a novel pathway linking BAG3 expression to enhanced PDAC metastasis, thus making BAG3 a potential target for intervention in pancreatic cancer.

Successive dilution enthalpies ( Δ H ( m N - 1 → m N ) ) of glycidol enantiomers (R-(+)-glycidol, S-(−)-glycidol) and the racemate (R/S-(±)-glycidol) in (dimethylformamide (DMF) + water) mixtures rich in water (mass fractions of DMF, w DMF = 0 to 0.25) have been determined respectively by isothermal titration calorimetry (ITC) at T = 298.15 K. The corresponding homotactic enthalpic pairwise interaction coefficients ( h XX ) of each compound have been evaluated from the framework of McMillan–Mayer theory. Across the studied composition range of (DMF + water) mixtures the h XX values of these compounds are all positive, and decrease gradually with the mass fraction of DMF by the order h RR > h RS ≈ h MM > h SS > 0 (M represents the racemate R/S-(±)-glycidol, and h RS is the estimated value for the heterochiral pair R–S). The positive values of h XX indicate that pairwise interactions of these compounds are endothermic and unfavourable from the point of view of enthalpy. The interaction of S–S pair is considered to be slightly stronger than M–M, R–S and R–R pairs since the former absorbs less heat than the latter in pairwise interactions. The addition of cosolvent (DMF) is in favour of pairwise interactions of these compounds in the mixtures rich in water.

Dilution enthalpies of six α-amino acid enantiomers (l-alanine vs d-alanine, l-serine vs d-serine, and l-proline vs d-proline) in pure water were determined at T = (288.15 to 323.15) K by isothermal titration calorimetry (ITC). Homochiral enthalpic pairwise interaction coefficients (hxx) at each temperature were evaluated according to the McMillan–Mayer theory. The hxx values of α-alanine and α-proline enantiomers are all positive (hLL > hDD > 0), while those of α-serine enantiomers are all negative (hLL < hDD < 0). In both cases, the hxx values increase uniformly and gradually with elevating temperatures. A slight but significant enthalpic discrimination effect is found in the homochiral pairwise interactions of these α-amino acid enantiomers. The positive growth of hxx values indicates that increasing temperature promotes the predominance of hydrophobic interactions in the binary aqueous solutions studied.

Context: BAG3 plays a regulatory role in a number of cellular processes. Recent studies have attracted much attention on its role in activation of selective autophagy. In addition, we have very recently reported that BAG3 is implicated in a BECN1-independent autophagy, namely noncanonical autophagy. Objective: The current study aimed to investigate the potential involvement of BAG3 in canonical autophagy triggered by Earle's Balanced Salt Solution (EBSS) starvation. Setting and Design: Replacement of complete medium with EBSS was used to trigger canonical autophagy. BAG3 expression was measured using real-time RT-PCR and Western blot. Autophagy was monitored using LC3-II transition and p62/SQSTM1 accumulation by Western blot, as well as punctate distribution of LC3 by immunofluorescence staining. Cell growth and apoptotic cell death was investigated using real-time cell analyzer and flowcytometry, respectively. Results: BAG3 expression was potently reduced by EBSS starvation. Forced expression of BAG3 suppressed autophagy and promoted apoptotic cell death of thyroid cancer cells elicited by starvation. In addition, in the presence of autophagy inhibitor, the enhancing effect of BAG3 on apoptotic cell death was attenuated. Conclusions: These results suggest that BAG3 promotes apoptotic cell death in starved thyroid cancer cells, at least in part by autophagy attenuation.

The epithelial–mesenchymal transition (EMT) of tubular epithelial cells to myofibroblast-like cells plays a substantial role in renal tubulointerstitial fibrosis, which is a common pathological character of end-stage renal disease (ESRD). Fibroblast growth factor-2 (FGF-2) triggers EMT in tubular epithelial cells and increases Bcl-2-associated athanogene 3 (BAG3) expression in neural progenitor and neuroblastoma cells. In addition, a novel role of regulation of EMT has been ascribed to BAG3 recently. These previous reports urged us to study the potential involvement of BAG3 in EMT triggered by FGF-2 in renal tubular epithelial cells. The current study found that FGF-2 induced EMT, simultaneously increased BAG3 expression in human kidney 2 (HK2) cells. Although FGF-2 induced EMT in nontransfected or scramble short hairpin RNA (shRNA) transfected HK2 cells, it was ineffective in BAG3-silenced cells, indicating a favorable role of BAG3 in EMT of tubular cells induced by FGF-2. Knockdown of BAG3 also significantly suppressed motion and invasion of HK2 cells mediated by FGF-2. Furthermore, we confirmed that BAG3 was upregulated in kidney of unilateral ureteral obstruction (UUO) rats, a well-established renal fibrosis model, in which EMT is supposed to exert a substantial influence on renal fibrosis. Importantly, upregulation of BAG3 was limited to tubular epithelial cells. Results of the current study identify BAG3 as a potential player in EMT of tubular epithelial cells, as well as renal fibrosis.

Although glomerular and vascular damage have been considered the main characteristics of diabetic kidney disease (DKD), accumulating data now indicate that tubular atrophy also plays a major role. Cathepsin D (CatD) is the major aspartate protease within lysosomes. The current study demonstrated that CatD expression was altered in the renal tubular epithelium in patients with diabetes mellitus (DM). In contrast to its low and uniform distribution in the tubular epithelium in normal kidney tissues, CatD demonstrated flecked and increased expression in tubules with relatively integral structures, and disappeared in disordered tubules in DM kidney tissues. In vitro studies demonstrated that CatD protected HK2 cells from the damage induced by high glucose and advanced glycation end-products (AGEs), independent of its enzymatic activity. In addition, the current study demonstrated that AGEs induced lysosome membrane permeabilization (LMP) and loss of mitochondrial membrane potential (MMP). Overexpression of CatD prevented LMP and maintained the MMP in HK2 cells exposed to AGEs. In addition, the catalytic activity of CatD was not required for its role in LMP prevention and MMP maintenance. These results indicate, for the first time that CatD may improve the viability of renal tubular cells in the presence of diabetic mediators independent of its enzymatic activity by preventing LMP and stabilizing the MMP.

Bcl-2 associated athanogene 3 (BAG3) contains a modular structure, through which BAG3 interacts with a wide range of proteins, thereby affording its capacity to regulate multifaceted biological processes. BAG3 is often highly expressed and functions as a pro-survival factor in many cancers. However, the oncogenic potential of BAG3 remains not fully understood. The cell cycle regulator, S-phase kinase associated protein 2 (Skp2) is increased in various cancers and plays an important role in tumorigenesis. The current study demonstrated that BAG3 promoted proliferation of ovarian cancer cells via upregulation of Skp2. BAG3 stabilized Skp2 mRNA via its 3'-untranslated region (UTR). The current study demonstrated that BAG3 interacted with Skp2 mRNA. In addition, miR-21-5p suppressed Skp2 expression, which was compromised by forced BAG3 expression. These results indicated that at least some oncogenic functions of BAG3 were mediated through posttranscriptional regulation of Skp2 via antagonizing suppressive action of miR-21-5p in ovarian cancer cells.

The dilution enthalpies of four 2′-deoxynucleosides, namely 2′-deoxyuridine (dU), 2′-deoxycytidine (dC), 2′-deoxyguanosine (dG) and 2′-deoxythymidine (dT), in (dimethylsulfoxide (DMSO) + water) mixtures of various mass fractions (wDMSO = 0 to 0.30) have been determined at T = 298.15 K, respectively, using an isothermal titration calorimeter (ITC200 MicroCal). On the basis of McMillan–Mayer’ theory, enthalpic pair wise self-interaction coefficients (hxx) of each compound at different values of wDMSO have been evaluated from successive dilution enthalpies. It was found that the values of hxx are all large negative and increase gradually with wDMSO across the whole composition range of the mixed solvent studied, though the degree of variation among them is somewhat different. The results indicate that (hydrophilic + hydrophilic) interactions are prevailing over (hydrophobic + hydrophobic) and (hydrophobic + hydrophilic) interactions in the ternary aqueous solutions under study.

The dilution enthalpies of nicotinamide (NA) and isonicotinamide (INA) in (dimethyl sulfoxide (DMSO) + water) and (dimethylformamide (DMF) + water) mixed solvents (M1 and M2) at 298.15 K have been determined, respectively, using an isothermal titration calorimeter (MicroCal ITC200). On the basis of the McMillan-Mayer theory, enthalpic pairwise self-interaction coefficients (hxx) of NA and INA in both M1 and M2 aqueous mixed solvents (mole fractions of cosolvents xcos = 0 to 0.10) have been calculated. It was found that the values of hxx are all large negative, with the relative magnitudes hxx(NA) hxx (in M2) for both NA and INA, and that all of them increase monotonously with the concentrations of cosolvents (both DMF and DMSO). It implies that an intense exothermic effect accompanies with the pairwise hydrophilic–hydrophilic self-interactions, in which the meso-isomer (NA) behaves as a stronger molecular associator than the para-isomer (INA).

Bcl-2 associated athanogene 3 (BAG3) has a modular structure that contains a BAG domain, a WW domain, a proline-rich (PxxP) domain to mediate potential interactions with chaperons and other proteins that participate in more than one signal transduction. In search for novel interacting partners, the current study identified that 78kDa glucose-regulated protein (GRP78) was a novel partner interacting with BAG3. Interaction between GRP78 and BAG3 was confirmed by coimmunoprecipitation and glutathione S-transferase (GST) pulldown. We also identified that the ATPase domain of GRP78 and BAG domain of BAG3 mediated their interaction. Counterintuitive for a prosurvival protein, BAG3 was found to promote the cytotoxicity of breast cancer MCF7, thyroid cancer FRO and glioma U87 cells subjected to genotoxic stress. In addition, the current study demonstrated that BAG3 interfered with the formation of the antiapoptotic GRP78-procaspase-7 complex, which resulted in an increased genotoxic stress-induced cytotoxicity in cancer cells. Furthermore, overexpression of GRP78 significantly blocked the enhancing effects of BAG3 on activation of caspase-7 and induction of apoptosis by genotoxic stress. Overall, these results suggested that through direct interaction BAG3 could prevent the antiapoptotic effect of GRP78 upon genotoxic stress.

BAG3 plays a regulatory role in a number of cellular processes, including cell proliferation, apoptosis, adhesion and migration, epithelial–mesenchymal transition (EMT), autophagy activation, and virus infection. The AP-1 transcription factors are implicated in a variety of important biological processes including cell differentiation, proliferation, apoptosis and oncogenesis. Recently, it has been reported that AP-1 protein c-Jun inhibits autophagy and enhances apoptotic cell death mediated by starvation. However, the molecular mechanisms remain unclear. For the first time, the current study demonstrated that serum starvation downregulated BAG3 at the transcriptional level via c-Jun. In addition, the current study reported that BAG3 stabilized JunD mRNA, which was, at least in part, responsible for the promotion of serum starvation mediated-growth inhibition by BAG3.

Proteasome inhibitors represent a novel class of anticancer agents that are used in the treatment of hematologic malignancies and various solid tumors. However, mechanisms underlying their anticancer actions were not fully understood. It has been reported that strong 14‐3‐3 protein expression is observed and associated with tumor genesis and progression of astrocytoma. In addition, global inhibition of 14‐3‐3 functions with a general 14‐3‐3 antagonist difopein induces apoptosis of human astrocytoma cells, validating 14‐3‐3 as a potential molecular target for anticancer therapeutic management. In the current study, for the first time we demonstrated that proteasome inhibitors downregulated 14‐3‐3ε and 14‐3‐3θ/τ in U87 and SF295 glioma cells. Overexpression of 14‐3‐3ε and 14‐3‐3θ/τ significantly suppressed apoptosis of human glioma cells induced by proteasome inhibitors. We also demonstrated that MG132 activated ASK1 and siASK1 compromised the MG132‐induced apoptosis of glioma cells. Furthermore, overexpression of 14‐3‐3ε and 14‐3‐3θ/τ markedly suppressed activation of ASK1. Collectively, the current study supported that proteasome inhibitors, at least in part, caused cytotoxicity of glioma cells via downregulation of 14‐3‐3ε and 14‐3‐3θ/τ and subsequent activation of ASK1. (Cancer Sci 2013; 104: 55–61)

Protein kinase C delta (PKCδ) is a serine (Ser)/threonine kinase, which regulates numerous cellular processes, including proliferation, differentiation, migration and apoptosis. In the current study, Chinese hamster ovary cells were transfected with either a constitutively activated PKCδ or a dominant negative PKCδ, phosphoprotein enrichment, two-dimensional difference gel electrophoresis and mass spectrometry was combined to globally identified candidates of PKCδ cascade. We found that Bcl-2 associated athanogene 3 (BAG3) was one of the targets of PKCδ cascade, and BAG3 interacted with PKCδ in vivo. In addition, we clarified that BAG3 was phosphorylate at Ser187 site in a PKCδ-dependent manner in vivo. BAG3 has been implicated in multiple cellular functions, including proliferation, differentiation, apoptosis, migration, invasion, macroautophagy and so on. We generated wild-type (WT)-, Ser187Ala (S187A)- or Ser187Asp (S187D)-BAG3 stably expressing FRO cells, and noticed that phosphorylation state of BAG3 influenced FRO morphology. Finally, for the first time, we showed that BAG3 was implicated in epithelial-mesenchymal transition (EMT) procedure, and phosphorylation state at Ser187 site had a critical role in EMT regulation by BAG3. Collectively, the current study indicates that BAG3 is a novel substrate of PKCδ, and PKCδ-mediated phosphorylation of BAG3 is implicated in EMT and invasiveness of thyroid cancer cells.

Proteasome inhibition may cause endoplasmic reticulum (ER) stress, which has been reported to be implicated in the antitumoral effects of proteasome inhibitors. CCAAT/enhancer‐binding protein homologous protein (CHOP) is induced by a variety of adverse physiological conditions including ER stress and is involved in apoptosis. We have reported that distinct induction of CHOP contributes to the responsiveness of thyroid cancer cells to proteasome inhibitors. However, the mechanism underlying differential induction of CHOP by proteasome inhibitors in thyroid cancer cells has not been well characterized. In the current study, we characterized that proteasome inhibition primarily activated the amino acid response element 1 (AARE1) on the CHOP promoter. We also demonstrated that although proteasome inhibition caused similar accumulation of activating transcription factor 4 (ATF4) in a panel of thyroid cancer cells, distinct amounts of ATF4 were recruited to the AARE1 element of CHOP promoter. In addition, we demonstrated that NF‐E2‐related factor 2 (Nrf2) was also implicated in the induction of CHOP by precluding the binding of ATF4 to the CHOP promoter. This study highlights the molecular mechanisms by which ATF4 and Nrf2 can control CHOP induction in thyroid cancer cells by proteasome inhibition.

Lipopolysaccharide (LPS) is an outer-membrane glycolipid component of Gram-negative bacteria known for its fervent ability to activate monocytic cells and for its potent proinflammatory capabilities. Bcl-2-associated athanogene 3 (BAG3) is a survival protein that has been shown to be stimulated during cell response to stressful conditions, such as exposure to high temperature, heavy metals, proteasome inhibition, and human immunodeficiency virus 1 (HIV-1) infection. In addition, BAG3 regulates replication of Varicella-Zoster Virus (VZV) and Herpes Simplex Virus (HSV) replication, suggesting that BAG3 could participate in the host response to infection. In the current study, we found that LPS increased the expression of BAG3 in a dose- and time-dependent manner. Actinomycin D completely blocked the LPS-induced BAG3 accumulation, as well as LPS activated the proximal promoter of BAG3 gene, supported that the induction by LPS occurred at the level of gene transcription. LPS-induced BAG3 expression was blocked by JNK or NF-κB inhibition, suggesting that JNK and NF-κB pathways participated in BAG3 induction by LPS. In addition, we also found that induction of BAG3 was implicated in monocytic cell adhesion to extracellular matrix induced by LPS. Overall, the data support that BAG3 is induced by LPS via JNK and NF-κB-dependent signals, and involved in monocytic cell-extracellular matrix interaction, suggesting that BAG3 may have a role in the host response to LPS stimulation.

Our previous data showed that reactive oxygen species generation might be ascribed to the cytotoxic response of thyroid cancer cells to proteasome inhibition and the ability of cancer cells to induce catalytic subunit for glutamate cysteine ligase (GCLC) and subsequent production of glutathione, thereby scavenging reactive oxygen species was partly ascribed to the cytotoxic responses of thyroid cancer cells to proteasome inhibition. Nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor responsible for transcriptional activation of various cytoprotective genes including GCLC.The purpose of this study was to determine the involvement of Nrf2 in GCLC induction and cytotoxicity of thyroid cancer cells mediated by proteasome inhibition.The effects of proteasome inhibition on the expression and distribution of Nrf2 were analyzed using immunocytochemistry and Western blot. To ascertain the effect of Nrf2 and p38 MAPK, cells were transfected with Nrf2 plasmid or small interfering RNA against Nrf2 or p38 MAPK. Apoptotic cells, production of glutathione, and induction of GCLC mediated by proteasome inhibition were investigated using flow cytometry, spectrophotometry, and real-time RT-PCR, respectively.Proteasome inhibition caused accumulation and nuclear translocation of Nrf2, which compromised the cytotoxic effects of proteasome inhibition, at least in part, via induction of GCLC. In addition, nuclear translocation of Nrf2 was p38 MAPK dependent, and p38 MAPK inhibition augmented the cytotoxic effects of proteasome, at least partly, via suppression of transactivation of Nrf2.These studies support the hypothesis that proteasome inhibitors activate an antiapoptotic survival program through p38 MAPK that involves transcriptional activity of Nrf2.

Proteasome inhibitors represent a novel class of antitumor agents with pre-clinical and clinical evidence of activity against hematologic malignancies and solid tumors. However, emerging evidence indicates that antiapoptotic factors may also accumulate as a consequence of exposure to these drugs, thus it seems plausible that the activation of survival signaling cascades might compromise their antitumoral effects. Peroxiredoxins (PRDXs) are a family of thiol-containing peroxidases identified primarily by their ability to remove cellular hydroperoxides. The function of PRDX1 in particular has been implicated in regulating cell proliferation, differentiation, and apoptosis. Another important finding is that aberrant upregulation of PRDX1 has been discovered in various cancers. Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase (MAPK) kinase kinase that is regulated under conditions of cellular stress. ASK1 phosphorylates c-Jun N-terminal kinase and p38 MAPK, and elicits an apoptotic response. ASK1 activity is regulated at multiple levels, one of which is through interaction with PRDX1. In this study, for the first time we report that upregulation of PRDX1 expression was found in thyroid cancer cells treated with proteasome inhibitors, and PRDX1 knockdown resulted in accelerated proteasome inhibitor-induced cell death. In addition, we demonstrated that ASK1 activity was implicated in the PRDX1-dependent response of thyroid cancer cells to proteasome inhibitor-mediated cell death.

The cobalt, nickel, copper, zinc and cadmium complexes of S-methyl-N-(ferrocenyl-1-methyl-methylidene)-dithiocarbazate (H-LSM) and S-benzyl-N-(ferrocenyl-1-methyl-methylidene)-dithiocarbazate (H-LSB) were synthesized and the crystal structure of Cd[Fe-C(CH3) = NNCSS-(CH3)]2 was solved by X-ray diffraction. The crystal is in the orthorhombic system with space group Pbca, cell parameters a=19.741(3), b=19.924(5), c=15.452(4) A, and the final factors of R=0.032. The study on quenching the luminescence of Ru(bpy)2+3 by those complexes showed that bimolecular quenching constants obtained from the Stern-Volmer constant and the excited-state lifetime were related to the redox potential of the quencher. Linear relationship is shown in the plot of logkq vs. E1/2(Q+/Q). The main factor which influences the quenching rate constant and the redox potential is the coordinating ability of the metal in the complex.

The copper(II) complex[Cu3(nta)2(azpy)2(H2O)2]·6H2O (nta = nitrilotriacetate, azpy = 4,4′-azobispyridine) has been synthesized and characterized. The X-ray analysis reveals that there are two kinds of copper(II) coordination environments. Cu(1) has a distorted square plane symmetry and Cu(2) has a distorted octahedral symmetry. Cu(1) is linked to Cu(2) through nta and bound to Cu(1C) by azpy, and Cu(2) is linked to Cu(2A) through azpy, which extends to two-dimensional network with large rhombus 1.2 nm × 1.7 nm.

The non-ionic europium(III) complex [Eu(TTA)3·DAF]·0.5C7H8 (TTA = 2-thenoytrifluoroacetonate, DAF = 4, 5-diazafluoren-9-one) was synthesized. The structural determination has been carried out. DAF coordination induces the both excitation spectra in the solid state and solution having a red shift and sensitizes Eu3+ luminescence under visible light excitation.