Interpenetrated Lattices of Quaternary Chalcogenides Displaying Magnetic Frustration, High Na-Ion Conductivity, and Cation Redox in Na-Ion Batteries.

A series of quaternary selenides, NaxMGaSe4 (M = Mn, Fe, and mixed Zn/Fe), have been synthesized for the first time employing a high-temperature solid-state synthesis route through stochiometric or polychalcogenide flux reactions. Along with the selenides, a previously reported sulfide analogue, NaxFeGaS4, is also revisited with new findings. These compounds form an interpenetrated structure made up of a supertetrahedral unit. The electrochemical evaluations exhibit a reversible (de)intercalation of ∼0.6 and ∼0.45 Na-ions, respectively, from Na2.87FeGaS4 (1a) and Na2.5FeGaSe4 (2) involving Fe2+/Fe3+ redox when cycled between 1.5 and 2.5 V. Mössbauer spectroscopy of 1a shows the existence of a mixed oxidation state of Fe2+/3+ in the pristine compound and reversible oxidation of Fe2+ to Fe3+ during the electrochemical cycles. Na2.79Zn0.6Fe0.4GaSe4 possesses a reasonably high room temperature ionic conductivity of 0.077 ms/cm with an activation energy of 0.30 eV. The preliminary magnetic measurements show a bifurcation of FC-ZFC at 4.5 and 2.5 K, respectively, for 1a and Na3MnGaSe4 (4) arising most likely from a spin-glass like transition. The high negative values of the Weiss constants -368.15 and -308.43 K for 1a and 4, respectively, indicate strong antiferromagnetic interactions between the magnetic ions and also emphasize the presence of a high degree of magnetic frustration in these compounds.

NaGaSe2: A Water-Loving Multifunctional Non-van der Waals Layered Selenogallate.

A missing member of well-known ternary chalcometallates, a sodium selenogallate, NaGaSe2, has been synthesized by employing a polyselenide flux and stoichiometric reaction. Crystal structure analysis using X-ray diffraction techniques reveals that it contains supertetrahedral adamantane-type Ga4Se10 secondary building units. These Ga4Se10 secondary building units are further connected via corners to form two-dimensional (2D) [GaSe2]∞- layers stacked along the c-axis of the unit cell, and the Na ions reside in the interlayer space. The compound has an unusual ability to absorb water molecules from the atmosphere or a nonanhydrous solvent to form distinct hydrated phases, NaGaSe2·xH2O (where x can be 1 and 2), with an expanded interlayer space, as verified by X-ray diffraction (XRD), thermogravimetric-differential scanning calorimetry (TG-DSC), desorption, and Fourier transform infrared spectroscopy (FT-IR) studies. The in situ thermodiffractogram indicates the emergence of an anhydrous phase before 300 °C with the decrease of interlayer spacings and reverting to the hydrated phase within a minute of re-exposure to the environment, supporting the reversibility of such a process. Structural transformation induced through water absorption results in an increase of Na ionic conductivity by 2 orders of magnitude compared to that of the pristine anhydrous phase, as verified by impedance spectroscopy. Na ions from NaGaSe2 can be exchanged in the solid-state route with other alkali and alkaline earth metals in a topotactic or nontopotactic way, leading to 2D isostructural and three-dimensional networks, respectively. Optical band gap measurements show a band gap of ∼3 eV for the hydrated phase, NaGaSe2·xH2O, which is in good agreement with the calculated band gap using a density functional theory (DFT)-based method. Sorption studies further confirm the selective absorption of water over MeOH, EtOH, and CH3CN with a maximum water uptake of 6 molecules/formula unit at a relative pressure, P/P0, of 0.9.

Lithium selenometallates of triel elements, Li5MSe4 (M = Al and Ga), aliovalent doping and their ionic conductivity.

Ternary selenometallates, Li5MSe4 (M = Al(I) and Ga(II)), have been synthesized for the first time through high temperature solid-state reactions combining elements and Li2Se in stoichiometric compositions. Li5MSe4 crystallizes in the P21/m space group, forming a pseudo-2D layer type structure with edge sharing LiSe4 and MSe4 tetrahedra along the a-axis. These layers are interleaved by octahedrally coordinated Li ions located in the interlayer space. AC impedance spectroscopy measurements yield room temperature ionic conductivities of 0.60 × 10-7 and 0.58 × 10-7 S cm-1 with calculated activation energies of 0.51 and 0.48 eV for I and II, respectively. An aliovalent substitution of Sn4+ in Li5MSe4 yields compositions of Li4.66Al0.82Sn0.22Se4 (III) and Li4.37Ga0.89Sn0.24Se4 (IV), which crystallize in the P21/m and P3̄m1 space groups, respectively. Sn-doped samples show an ∼5-fold increase in ionic conductivity, 3.37 × 10-7 S cm-1 and 2.4 × 10-7 S cm-1 with activation energies of 0.54 and 0.28 eV, respectively, for III and IV. The optical band gap values of the compounds are 3.65 and 3.2 eV for I and II, respectively, as measured by diffuse reflectance spectroscopy. Density functional theory (DFT) calculations predicted a major contribution from the Se 4p-states in forming the top of the valence band and strongly hybridized the Se 4p and ns orbitals of Al and Ga in forming the bottom of the conduction band with almost no contribution from the Li s-states near the Fermi level indicating their ionic interactions with the ligand.

Waste Toner-Derived Carbon/Fe3O4 Nanocomposite for High-Performance Supercapacitor.

Electronic waste management is one of the key challenges for the green revolution without affecting the environment. The wide use of printer devices has brought a horde of discarded waste toner, which release ∼6000 tons of processed carbon powder into the atmosphere every year that would essentially pollute the atmosphere. Here, we propose a one-step thermal conversion of waste toner powder into carbon/Fe3O4 nanocomposites for energy storage applications. Recovered toner carbon (RTC) and toner carbon calcined at 300 °C (RTC-300) were characterized using various analytical tools. From the FE-SEM analysis, the presence of carbon particles with uniformly decorated Fe3O4 nanoparticles was confirmed. RTC-300 carbon was used as an electrode material for supercapacitors, and it exhibited a high specific capacitance of 536 F/g at a current density of 3 A/g, which is almost six times higher than that of the commercial mesoporous graphitized carbon black. RTC-300 showed excellent electrochemical stability of 97% over 5000 cycles at a high current density of 20 A/g. The fabricated symmetric cell using RTC-300 electrode materials in an aqueous electrolyte with a cell voltage of 1.8 V delivered a high energy and high-power density of 42 W h/kg and 14.5 kW/kg, respectively. The fabricated device is stable up to 20,000 cycles at a high current density of 20 A/g with a loss of 23% capacitance.

Translational downregulation of Twist1 expression by antiproliferative gene, B-cell translocation gene 2, in the triple negative breast cancer cells.

Twist1, a key transcription factor regulating epithelial-mesenchymal transition and cancer metastasis, is highly expressed in invasive cancers in contrast to the loss of BTG2/TIS21 expression. Based on our observation that forced expression of BTG2/TIS21 downregulated Twist1 protein expression without altering mRNA level, we investigated molecular mechanisms of the BTG2/TIS21-inhibited Twist1 translation in the triple negative breast cancer (TNBC) cells and in vivo BTG2/TIS21-knockout (KO) mice and human breast cancer tissues. (1) C-terminal domain of Twist1 and Box B of BTG2/TIS21 interacted with each other, which abrogated Twist1 activity. (2) BTG2/TIS21 inhibited translational initiation by depleting eIF4E availability via inhibiting 4EBP1 phosphorylation. (3) Expression of BTG2/TIS21 maintained p-eIF2α that downregulates initiation of protein translation, confirmed by eIF2α-AA mutant expression and BTG2/TIS21 knockdown in MEF cells. (4) cDNA microarray analysis revealed significantly higher expression of initiation factors-eIF2A, eIF3A, and eIF4G2-in the BTG2/TIS21-KO mouse than that in the wild type. (5) BTG2/TIS21-inhibited translation initiation lead to the collapse of polysome formation and the huge peak of 80s monomer in the BTG2/TIS21 expresser, but not in the control. (6) mRNAs and protein expressions of elongation factors were also downregulated by BTG2/TIS21 expression in TNBC cells, but much higher in both TIS21-KO mice and lymph node-positive human breast cancers. (7) BTG2/TIS21-mediated Twist1 loss was not due to the protein degradation by ubiquitination and autophagy activation. (8) Twist1 protein level was significantly higher in various organs of TIS21-KO mice compared with that in the control, indicating the in vivo role of BTG2/TIS21 gene in the regulation of Twist1 protein level. Altogether, the present study support our hypothesis that BTG2/TIS21 is a promising target to combat with metastatic cancers with high level of Twist1 without BTG2/TIS21 expression.

TIS21/BTG2 inhibits breast cancer growth and progression by differential regulation of mTORc1 and mTORc2-AKT1-NFAT1-PHLPP2 signaling axis.

PURPOSE: It has been reported that PI3K/AKT pathway is altered in various cancers and AKT isoforms specifically regulate cell growth and metastasis of cancer cells; AKT1, but not AKT2, reduces invasion of cancer cells but maintains cancer growth. We propose here a novel mechanism of the tumor suppresser, TIS21/BTG2, that inhibits both growth and invasion of triple negative breast cancer cells via AKT1 activation by differential regulation of mTORc1 and mTORc2 activity. METHODS: Transduction of adenovirus carrying TIS21/BTG2 gene and transfection of short interfering RNAs were employed to regulate TIS21/BTG2 gene expression in various cell lines. Treatment of mTOR inhibitors and mTOR kinase assays can evaluate the role of mTORc in the regulation of AKT phosphorylation at S473 residue by TIS21/BTG2 in breast cancer cells. Open data and immunohistochemical analysis were performed to confirm the role of TIS21/BTG2 expression in various human breast cancer tissues. RESULTS: We observed that TIS21/BTG2 inhibited mTORc1 activity by reducing Raptor-mTOR interaction along with upregulation of tsc1 expression, which lead to significant reduction of p70S6K activation as opposed to AKT1S473, but not AKT2, phosphorylation via downregulating PHLPP2 (AKT1-specific phosphatase) in breast cancers. TIS21/BTG2-induced pAKTS473 required Rictor-bound mTOR kinase, indicating activation of mTORc2 by TIS21/BTG2 gene. Additionally, the TIS21/BTG2-induced pAKTS473 could reduce expression of NFAT1 (nuclear factor of activated T cells) and its target genes, which regulate cancer microenvironment. CONCLUSIONS: TIS21/BTG2 significantly lost in the infiltrating ductal carcinoma, but it can inhibit cancer growth via the TIS21/BTG2-tsc1/2-mTORc1-p70S6K axis and downregulate cancer progression via the TIS21/BTG2-mTORc2-AKT1-NFAT1-PHLPP2 pathway.

Inhibition of TNFα-interacting protein α (Tipα)-associated gastric carcinogenesis by BTG2/TIS21 via downregulating cytoplasmic nucleolin expression.

To understand the regulation of Helicobacter pylori (H. pylori)-associated gastric carcinogenesis, we examined the effect of B-cell translocation gene 2 (BTG2) expression on the biological activity of Tipα, an oncoprotein secreted from H. pylori. BTG2, the human ortholog of mouse TIS21 (BTG2/TIS21), has been reported to be a primary response gene that is transiently expressed in response to various stimulations. Here, we report that BTG2 is constitutively expressed in the mucous epithelium and parietal cells of the gastric gland in the stomach. Expression was increased in the mucous epithelium following H. pylori infection in contrast to its loss in human gastric adenocarcinoma. Indeed, adenoviral transduction of BTG2/TIS21 significantly inhibited Tipα activity in MKN-1 and MGT-40, human and mouse gastric cancer cells, respectively, thereby downregulating tumor necrosis factor-α (TNFα) expression and Erk1/2 phosphorylation by reducing expression of nucleolin, a Tipα receptor. Chromatin immunoprecipitation proved that BTG2/TIS21 inhibited Sp1 expression and its binding to the promoter of the nucleolin gene. In addition, BTG2/TIS21 expression significantly reduced membrane-localized nucleolin expression in cancer cells, and the loss of BTG2/TIS21 expression induced cytoplasmic nucleolin availability in gastric cancer tissues, as evidenced by immunoblotting and immunohistochemistry. Higher expression of BTG2 and lower expression of nucleolin were accompanied with better overall survival of poorly differentiated gastric cancer patients. This is the first report showing that BTG2/TIS21 inhibits nucleolin expression via Sp1 binding, which might be associated with the inhibition of H. pylori-induced carcinogenesis. We suggest that BTG2/TIS21 is a potential inhibitor of nucleolin in the cytoplasm, leading to inhibition of carcinogenesis after H. pylori infection.

B-cell translocation gene 2 mediates crosstalk between PI3K/Akt1 and NFκB pathways which enhances transcription of MnSOD by accelerating IκBα degradation in normal and cancer cells.

BACKGROUND: B-cell translocation gene 2 (BTG2) belongs to antiproliferative (ARPO) gene family and the expression of BTG2, human ortholog of rat PC3 and mouse TIS21 gene, has been shown to render cancer cells more sensitive to doxorubicin treatment by upregulating MnSOD expression without regulating any other reactive oxygen species (ROS) scavenging enzymes. RESULTS: In the present study, by employing exogenous and endogenous BTG2/TIS21/Pc3 expression by transfection and transduction analyses, and by knockdown of gene expression using RNA interference or using gene knockout cells, we observed that BTG2 increased the binding of activated NF-κB (p65/RelA) to the enhancer element of MnSOD gene in the 2nd intron, which was regulated by p-Akt1, and the induction of MnSOD by BTG2 was accompanied with subsequent downregulation of ROS level and cyclin B1 biosynthesis along with the increase of p21WAF1, resulting in the G2/M arrest independent of p53. CONCLUSIONS: These results show for the first time that BTG2 mediates crosstalk between PI3K-Akt1 and NF-κB pathways, which regulates p53-independent induction of G2/M phase arrest both in normal and cancer cells.