Retraction Notice to: Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling.

[This retracts the article DOI: 10.1016/j.omtn.2018.03.002.].

Defect Passivation Effect of Chemical Groups on Perovskite Solar Cells.

Defect passivation is a key strategy to prepare high-performance perovskite solar cells (PVSCs). Even though abundant passivation molecules have been applied, the absence of detailed researches with regard to different functional groups in polymer additives may inevitably impede the establishment of passivation molecules selection rules. In this work, three passivation molecules including poly(vinyl alcohol) (PVA), polymethyl acrylate (PMA), and poly(acrylic acid) (PAA) are employed to systematically analyze the passivation effect from hydroxyl, carbonyl, and carboxyl groups. In general, PVA (-OH) can form hydrogen bonds with perovskite and PMA (-C═O) can complex with uncoordinated Pb2+. Specifically, PAA (-COOH) can interact selectively with MA+ and I- ions via hydrogen bonding and complex with uncoordinated Pb2+ to passivate defects more effectively. Hence, the PAA-incorporated PVSCs based on MAPbI3 achieve the champion power conversion efficiency (PCE) of 20.29% with open-circuit voltage up to 1.13 V. In addition, PAA cross-linking perovskite grains can relieve mechanical stress, as well as occupy the major channels to suppress ion migration and water/oxygen erosion. The corresponding unencapsulated devices demonstrate a superior light soaking stability, retaining more than 80% of the original PCE under one sun illumination for 1000 h.

Ionic Liquid-Induced Ostwald Ripening Effect for Efficient and Stable Tin-Based Perovskite Solar Cells.

Tin-based perovskite solar cells (PVSCs) are regarded as the most promising alternative among lead-free PVSCs. However, the rapid crystallization for tin-based perovskite tends to cause inferior film morphology and abundant defect states, which make poor photovoltaic performance. Here, 1-butyl-3-methylimidazolium bromide (BMIBr) ionic liquids (ILs) with strong polarity and a low melting point are first employed to produce the Ostwald ripening effect and obtain high-quality tin-based perovskite films with a large grain size. Meanwhile, the non-radiative recombination ascribed from defect states can also be effectively reduced for BMIBr-treated perovskite films. Consequently, a photoelectric conversion efficiency (PCE) of 10.09% for inverted tin-based PVSCs is attained by the Ostwald ripening effect. Moreover, the unencapsulated devices with BMIBr retain near 85% of the original PCE in a N2 glovebox beyond 1200 h and about 40% of the original PCE after exposure to air for 48 h.

Controlling Crystal Growth via an Autonomously Longitudinal Scaffold for Planar Perovskite Solar Cells.

Sequential deposition is certified as an effective technology to obtain high-performance perovskite solar cells (PVSCs), which can be derivatized into large-scale industrial production. However, dense lead iodide (PbI2 ) causes incomplete reaction and unsatisfactory solution utilization of perovskite in planar PVSCs without mesoporous titanium dioxide as a support. Here, a novel autonomously longitudinal scaffold constructed by the interspersion of in situ self-polymerized methyl methacrylate (sMMA) in PbI2 is introduced to fabricate efficient PVSCs with excellent flexural endurance and environmental adaptability. By this strategy perovskite solution can be confined within an organic scaffold with vertical crystal growth promoted, effectively inhibiting exciton accumulation and recombination at grain boundaries. Additionally, sMMA cross-linked perovskite network can release mechanical stress and occupy the main channels for ion migration and water/oxygen permeation to significantly improve operational stability, which opens up a new strategy for the commercial development of large-area PVSCs in flexible electronics.

Regulated Crystallization of Efficient and Stable Tin-Based Perovskite Solar Cells via a Self-Sealing Polymer.

Tin-based perovskite solar cells (PVSCs) have emerged as the most promising lead-free perovskite materials owing to their superior optoelectronic properties. However, the deficiency of accurate control of the tin-based perovskite crystallization process increases the possibility of unexpected perovskite film morphology and defects, resulting in inferior power conversion efficiency (PCE). Meanwhile, the poor environmental stability of tin-based perovskite films hinders its further development. In this work, a unique polymer [poly(ethylene-co-vinyl acetate) (EVA)] is introduced into anti-solvent during spin coating of formamidinium tin tri-iodide (FASnI3) precursor solution. The C═O groups contained in EVA have a powerful Lewis acid-base complexation with uncoordinated tin atoms in perovskite grains, which can greatly improve the grain size, optimize the grain orientation, and decrease the surface defects of FASnI3 films. This strategy offers an impressive PCE of 7.72% with favorable reproducibility. More importantly, the PVSC devices based on FASnI3-EVA absorbers have a self-encapsulation effect, which exhibits distinguished moisture and oxygen barrier property, thereby retaining 62.4% of the original efficiency value after aging for 48 h in the air with a humidity of 60%. Such a convenient strategy provides a new inspiration for the establishment of stable and high-performance tin-based PVSCs.

Preparation of efficient inverted tin-based perovskite solar cells via the bidentate coordination effect of 8-hydroxyquinoline.

The N and O atoms in the bidentate ligand 8-hydroxyquinoline (8-HQ) can simultaneously coordinate with Sn2+, which greatly inhibits the oxidation of Sn2+. The formation of complexes improves the quality of FASnI3 films and reduces defect states, resulting in improvements in the efficiency and stability of FASnI3-based perovskite solar cells.

Inflammatory-Related P62 Triggers Malignant Transformation of Mesenchymal Stem Cells through the Cascade of CUDR-CTCF-IGFII-RAS Signaling.

Inflammatory and autophagy-related gene P62 is highly expressed in most human tumor tissues. Herein, we demonstrate that P62 promotes human mesenchymal stem cells' malignant transformation via the cascade of P62-tumor necrosis factor alpha (TNF-α)-CUDR-CTCF-insulin growth factor II (IGFII)-H-Ras signaling. Mechanistically, we reveal P62 enhances IGFII transcriptional activity through forming IGFII promoter-enhancer chromatin loop and increasing METTL3 occupancy on IGFII 3' UTR and enhances H-Ras overexpression by harboring inflammation-related factors, e.g., TNFR1, CLYD, EGR1, NFκB, TLR4, and PPARγ. Furthermore, the P62 cooperates with TNF-α to promote malignant transformation of mesenchymal stem cells. These findings, for the first time, provide insight into the positive role that P62 plays in malignant transformation of mesenchymal stem cells and reveal a novel link between P62 and the inflammation factors in mesenchymal stem cells.

miR372 Promotes Progression of Liver Cancer Cells by Upregulating erbB-2 through Enhancement of YB-1.

MicroRNAs are known to be involved in carcinogenesis. Recently, microRNA-372 (miR372) has been proven to play a substantial role in several human cancers, but its functions in liver cancer remain unclear. Herein, our results demonstrate that miR372 accelerates growth of liver cancer cells in vitro and in vivo. Mechanistically, miR372 enhances expression of Y-box-binding protein 1 (YB-1) by targeting for phosphatase and tensin homolog (PTEN) directly and consequently promotes phosphorylation of YB-1 via HULC looping dependent on ERK1/2 and PTEN. In particular, HULC knockdown or PTEN overexpression abrogated this miR372 action. Moreover, miR372 inhibits the degradation of ß-catenin dependent on phosphorylation of YB-1 and then enhances the expression and activity of pyruvate kinase M2 isoform (PKM2) by ß-catenin-LEF/TCF4 pathway. Furthermore, the loading of LEF/TCF4 on PKM2 promoter region was significantly increased in miR372 overexpressing Hep3B, and thus, glycolytic proton efflux rate (glycoPER) was significantly increased in rLV-miR372 group compared to the rLV group. Moreover, ß-catenin knockdown abrogates this function of miR372. Ultimately, miR372 promotes the expression of erbB-2 through PKM2-pH3T11-acetylation on histone H3 lysine 9 (H3K9Ac) pathway. Of significance, both YB-1 knockdown and erbB-2 knockdown abrogate oncogenic action of miR372. Our observations suggest that miR372 promotes liver cancer cell cycle progress by activating cyclin-dependent kinase 2 (CDK2)-cyclin E-P21/Cip1 complex through miR372-YB-1-ß-catenin-LEF/TCF4-PKM2-erbB-2 axis. This study elucidates a novel mechanism for miR372 in liver cancer cells and suggests that miR372 can be used as a novel therapeutic target of liver cancer.

Inflammatory factor receptor Toll-like receptor 4 controls telomeres through heterochromatin protein 1 isoforms in liver cancer stem cell.

Toll-like receptor 4 (TLR4) which acts as a receptor for lipopolysaccharide (LPS) has been reported to be involved in carcinogenesis. However, the regulatory mechanism of it has not been elucidated. Herein, we demonstrate that TLR4 promotes the malignant growth of liver cancer stem cells. Mechanistically, TLR4 promotes the expression of histone-lysine N-methyltransferase (SUV39 h2) and increases the formation of trimethyl histone H3 lysine 9-heterochromatin protein 1-telomere repeat binding factor 2 (H3K9me3-HP1-TRF2) complex at the telomeric locus under mediation by long non coding RNA urothelial cancer-associated 1 (CUDR). At the telomeric locus, this complex promotes binding of POT1, pPOT1, Exo1, pExo1, SNM1B and pSNM1B but prevents binding of CST/AAF to telomere, thus controlling telomere and maintaining telomere length. Furthermore, TLR4 enhances interaction between HP1α and DNA methyltransferase (DNMT3b), which limits RNA polymerase II deposition on the telomeric repeat-containing RNA (TERRA) promoter region and its elongation, thus inhibiting transcription of TERRA. Ultimately, TLR4 enhances the telomerase activity by reducing the interplay between telomerase reverse transcriptase catalytic subunit (TERT) and TERRA. More importantly, our results reveal that tri-complexes of HP1 isoforms (α, ß and γ) are required for the oncogenic action of TLR4. This study elucidates a novel protection mechanism of TLR4 in liver cancer stem cells and suggests that TLR4 can be used as a novel therapeutic target for liver cancer.

Long noncoding RNA MEG3 suppresses liver cancer cells growth through inhibiting ß-catenin by activating PKM2 and inactivating PTEN.

Maternally expressed gene 3 (MEG3) encodes an lncRNA which is suggested to function as a tumor suppressor and has been showed to involve in a variety of cancers. Herein, our findings demonstrate that MEG3 inhibits the malignant progression of liver cancer cells in vitro and in vivo. Mechanistically, MEG3 promotes the expression and maturition of miR122 which targets PKM2. Therefore, MEG3 decreases the expression and nuclear location of PKM2 dependent on miR122. Furthermore, MEG3 also inhibits CyclinD1 and C-Myc via PKM2 in liver cancer cells. On the other hand, MEG3 promotes ß-catenin degradation through ubiquitin-proteasome system dependent on PTEN. Strikingly, MEG3 inhibits ß-catenin activity through PKM2 reduction and PTEN increase. Significantly, we also found that excessive ß-catenin abrogated the effect of MEG3 in liver cancer. In conclusion, our study for the first time demonstrates that MEG3 acts as a tumor suppressor by negatively regulating the activity of the PKM2 and ß-catenin signaling pathway in hepatocarcinogenesis and could provide potential therapeutic targets for the treatment of liver cancer.

HistoneH3 demethylase JMJD2A promotes growth of liver cancer cells through up-regulating miR372.

Changes in histone lysine methylation status have been observed during cancer formation. JMJD2A protein is a demethylase that is overexpressed in several tumors. Herein, our results demonstrate that JMJD2A accelerates malignant progression of liver cancer cells in vitro and in vivo. Mechanistically, JMJD2A promoted the expression and mature of pre-miR372 epigenetically. Notably, miR372 blocks the editing of 13th exon-introns-14th exon and forms a novel transcript( JMJD2AΔ) of JMJD2A. In particular, JMJD2A inhibited P21(WAF1/Cip1) expression by decreasing H3K9me3 dependent on JMJD2AΔ. Thereby, JMJD2A could enhance Pim1 transcription by suppressing P21(WAF1/Cip1). Furthermore, through increasing the expression of Pim1, JMJD2A could facilitate the interaction among pRB, CDK2 and CyclinE which prompts the transcription and translation of oncogenic C-myc. Strikingly, JMJD2A may trigger the demethylation of Pim1. On the other hand, Pim1 knockdown and P21(WAF1/Cip1) overexpression fully abrogated the oncogenic function of JMJD2A. Our observations suggest that JMJD2A promotes liver cancer cell cycle progress through JMJD2A-miR372-JMJD2AΔ-P21WAF1/Cip1-Pim1-pRB-CDK2-CyclinE-C-myc axis. This study elucidates a novel mechanism for JMJD2A in liver cancer cells and suggests that JMJD2A can be used as a novel therapeutic targets of liver cancer.

Inflammatory cytokine IL6 cooperates with CUDR to aggravate hepatocyte-like stem cells malignant transformation through NF-κB signaling.

Inflammatory cytokines and lncRNAs are closely associated with tumorigenesis. Herein, we reveal inflammatory cytokines IL6 cooperates with long noncoding RNA CUDR to trigger the malignant transformation of human embryonic stem cells-derived hepatocyte-like stem cells. Mechanistically, IL6 cooperates with CUDR to cause MELLT3 to interact with SUV39h1 mRNA3'UTR and promote SUV39h1 expression. Moreover, the excessive SUV39h1 also increases tri-methylation of histone H3 on nineth lysine (H3K9me3). Intriguingly, under inflammatory conditions, H3K9me3 promotes the excessive expression and phosphorylation of NF-κB, and in turn, phorsphorylated NF-κB promotes the expression and phosphorylation of Stat3. Furthermore, that the phosphorylated Stat3 loads onto the promoter region of miRs and lncRNAs. Ultimately, the abnormal expression of miRs and lncRNAs increased telomerase activity, telomere length and microsatellite instability (MSI), leading to malignant transformation of hepatocyte-like stem cells.

HULC cooperates with MALAT1 to aggravate liver cancer stem cells growth through telomere repeat-binding factor 2.

The dysregulation of lncRNAs has increasingly been linked to many human diseases, especially in cancers. Our results demonstrate HULC, MALAT1 and TRF2 are highly expressed in human hepatocellular carcinoma tissues, and HULC plus MALAT1 overexpression drastically promotes the growth of liver cancer stem cells. Mechanistically, both HULC and MALAT1 overexpression enhanced RNA polII, P300, CREPT to load on the promoter region of telomere repeat-binding factor 2(TRF2), triggering the overexpression, phosphorylation and SUMOylation of TRF2. Strikingly, the excessive TRF2 interacts with HULC or MALAT1 to form the complex that loads on the telomeric region, replacing the CST/AAF and recruiting POT1, pPOT1, ExoI, SNM1B, HP1 α. Accordingly, the telomere is greatly protected and enlonged. Furthermore, the excessive HULC plus MALAT1 reduced the methylation of the TERC promoter dependent on TRF2, increasing the TERC expression that causes the increase of interplay between TRET and TERC. Ultimately, the interaction between RFC and PCNA or between CDK2 and CyclinE, the telomerase activity and the microsatellite instability (MSI) are significantly increased in the liver cancer stem cells. Our demonstrations suggest that haploinsufficiency of HULC/MALAT1 plays an important role in malignant growth of liver cancer stem cell.

Inflammatory related gene IKKα, IKKß, IKKγ cooperates to determine liver cancer stem cells progression by altering telomere via heterochromatin protein 1-HOTAIR axis.

Cancer stem cells are associated with tumor recurrence. IKK is a protein kinase that is composed of IKKα, IKKß, IKKγ. Herein, we demonstrate that IKKα plus IKKß promoted and IKKγ inhibited liver cancer stem cell growth in vitro and in vivo. Mechanistically, IKKα plus IKKß enhanced and IKKγ inhibited the interplay among HP1α, HP1ß and HP1γ that competes for the interaction among HP1α, SUZ12, HEZ2. Therefore, IKKα plus IKKß inhibited and IKKγ enhanced the activity of H3K27 methyltransferase SUZ12 and EZH2, which methylates H3K27 immediately sites on HOTAIR promoter region. Therefore, IKKα plus IKKß increased and IKKγ decreased the HOTAIR expression. Strikingly, IKKα plus IKKß decreases and IKKγ increases the HP1α interplays with DNA methyltransferase DNMT3b, which increases or decreases TERRA promoter DNA methylation. Thus IKKα plus IKKß reduces and IKKγ increases to recruit TRF1 and RNA polymerase II deposition and elongation on the TERRA promoter locus, which increases or decreases TERRA expression. Furthermore, IKKα plus IKKß decreases/increases and IKKγ increases/decreases the interplay between TERT and TRRRA/between TERT and TREC. Ultimately, IKKα plus IKKß increases and IKKγ decreases the telomerase activity. On the other hand, at the telomere locus, IKKα plus IKKß increases/drcreases and IKKγ decreases/increases TRF2, POT1, pPOT1, Exo1, pExo1, SNM1B, pSNM1B/CST-AAF binding, which keep active telomere regulatory genes and poised for telomere length. Strikingly, HOTAIR is required for IKKα plus IKKß and IKKγ to control telomerase activity and telomere length. These observations suggest that HOTAIR operates the action of IKKα, IKKß, IKKγ in liver cancer stem cells. This study provides a novel basis to elucidate the oncogenic action of IKKα, IKKß, IKKγ and prompts that IKKα, IKKß, IKKγ cooperate to HOTAR to be used as a novel therapeutic targets for liver cancer.

Double mutant P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of Pim1 mediated by PKM2 and LncRNA CUDR.

P53 is frequently mutated in human tumors as a novel gain-of-function to promote tumor development. Although dimeric (M340Q/L344R) influences on tetramerisation on site-specific post-translational modifications of p53, it is not clear how dimeric (M340Q/L344R) plays a role during hepatocarcinogenesis. Herein, we reveal that P53 (N340Q/L344R) promotes hepatocarcinogenesis through upregulation of PKM2. Mechanistically, P53 (N340Q/L344R) forms complex with CUDR and the complex binds to the promoter regions of PKM2 which enhances the expression, phosphorylation of PKM2 and its polymer formation. Thereby, the polymer PKM2 (tetramer) binds to the eleventh threonine on histone H3 that increases the phosphorylation of the eleventh threonine on histone H3 (pH3T11). Furthermore, pH3T11 blocks HDAC3 binding to H3K9Ac that prevents H3K9Ac from deacetylation and stabilizes the H3K9Ac modification. On the other hand, it also decreased tri-methylation of histone H3 on the ninth lysine (H3K9me3) and increases one methylation of histone H3 on the ninth lysine (H3K9me1). Moreover, the combination of H3K9me1 and HP1 α forms more H3K9me3-HP1α complex which binds to the promoter region of Pim1, enhancing the expression of Pim1 that enhances the expression of TERT, oncogenic lncRNA HOTAIR and reduces the TERRA expression. Ultimately, P53 (N340Q/L344R) accerlerates the growth of liver cancer cells Hep3B by activating telomerase and prolonging telomere through the cascade of P53 (N340Q/L344R)-CUDR-PKM2-pH3T11- (H3K9me1-HP1α)-Pim1- (TERT-HOTAIR-TERRA). Understanding the novel functions of P53 (N340Q/L344R) will help in the development of new liver cancer therapeutic approaches that may be useful in a broad range of cancer types.

Gadolinium oxalate derivatives with enhanced magnetocaloric effect via ionothermal synthesis.

Two new oxalate-bridged Gd(III) coordination polymers, namely, (choline)[Gd(C2O4)(H2O)3Cl]Cl·H2O (1) and [Gd(C2O4)(H2O)3Cl] (2), were first obtained ionothermally by using a deep eutectic solvent (DES). The magnetic studies and heat capacity measurements reveal that the two-dimensional Gd(III)-based coordination polymer of 2 has the higher magnetic density and exhibits a larger cryogenic magnetocaloric effect (MCE) (ΔS(m) = 48 J kg(-1) K(-1) for ΔH = 7 T at 2.2 K).

Ionothermal synthesis of two oxalate-bridged lanthanide(III) chains with slow magnetization relaxation by using a deep eutectic solvent.

Two novel isostructural oxalate-bridged lanthanide(III) chains, (choline)[Ln(ox)(H2O)3Cl]Cl·H2O (Ln = Dy/Er), were first obtained ionothermally by using a choline chloride-oxalic acid eutectic mixture as both solvent and structure-directing agent, both of which show field-induced slow relaxation of magnetization.

A general synthetic method for MPO4 (M = Co, Fe, Mn) frameworks using deep-eutectic solvents.

A general approach was developed to synthesize a series of cobalt, manganese, and iron phosphate frameworks in deep-eutectic solvents through tuning important reaction parameters including temperature, time, and addition of water.

Mononuclear gold(I) acetylide complexes with urea group: synthesis, characterization, photophysics, and anion sensing properties.

A series of mononuclear gold(I) acetylide complexes with urea moiety, R'(3)PAuC≡CC(6)H(4)-4-NHC(O)NHC(6)H(4)-4-R (R' = cyclohexyl, R = NO(2) (2a), CF(3) (2b), Cl (2c), H (2d), CH(3) (2e), (t)Bu (2f), OCH(3) (2g); R' = phenyl, R = NO(2) (3a), OCH(3) (3b); R' = 4-methoxyphenyl, R = H (4a), OCH(3) (4b)), have been synthesized and characterized. The crystal structures of Ph(3)PAuC≡CC(6)H(4)-4-NHC(O)NHC(6)H(4)-4-NO(2) (3a) and (4-CH(3)OC(6)H(4))(3)PAuC≡CC(6)H(4)-4-NHC(O)NHC(6)H(5) (4a) have been determined by X-ray diffraction. Complexes 2a-2g, 3b, and 4a-4b show intense luminescence both in the solid state and in degassed THF solution at 298 K. Anion binding properties of complexes 2a-2g, 3a-3b, and 4a-4b have been studied by UV-vis and (1)H NMR titration experiments. In general, the log K values of 2a-2g with the same anion in THF depend on the substituent R on the acetylide ligand of 2a-2g: R = NO(2) (2a) > CF(3) (2b) ≥ Cl (2c) > H (2d) > CH(3) (2e) ≈ (t)Bu (2f) ≥ OCH(3) (2g). Complex 2a with NO(2) group shows the dramatic color change toward F(-) in DMSO, which provides an access of naked eye detection of F(-).

Two new 1,2,4,5-cyclohexanetetracarboxylate-bridged frameworks with metal hydroxide subunits. Synthesis, structures, magnetism and adsorption.

The hydrothermal synthesis, X-ray crystal structures and thermal and magnetic properties of a layered coordination polymer, [Ni(3.9)Mn(1.1)(µ(3)-OH)(2)(L(I))(2)(H(2)O)(10)]·2H(2)O (1) (L(I) = 1e,2a,4a,5e-cyclohexanetetracarboxylate), and a porous 3D coordination polymer, [Ni(4)(µ(2)-OH)(2)(µ(6)-H(2)L(IV))(2)(pymc)(4,4'-bpy)(H(2)O)(2)](OH)·9H(2)O (2) (pymc = 2-pyrimidinecarboxylate, 4,4'-bpy = 4,4'-bipyridine, L(IV) = 1e,2e,4e,5e-cyclohexanetetracarboxylate), are reported in this paper. The structure of 1 has packed separated layers, each layer being formed of M(3)(µ(3)-OH)(2) chains bridged by M(L(I))(2)via hydrogen bonds. The magnetic properties are characterized by Néel transitions to fully compensated antiferromagnets at 2.9 K and show that 1 is a metamagnet resulting from the ferrimagnetic M(3)(µ(3)-OH)(2) chains and other two metal atoms. Complex 2 is a 3D microporous coordination framework with 2D channels. The conformation of the 1,2,4,5-cyclohexanetetracarboxylate ligands (H(4)L) of complex 2 changes from L(I) (e,a,a,e) to L(IV) (e,e,e,e). The magnetic measurement indicates spin-canted antiferromagnetic behaviour, and the adsorption measurements show that 2 can selectively adsorb CO(2) gas over N(2) gas.