Four Honeycomb Metal–Organic Frameworks with a Flexible Tripodal Polyaromatic Acid

Reaction of 4,4′,4″-{[(2,4,6-trimethylbenzene-1,3,5-triyl)­tris­(methylene)]­tris­(oxy)}­tribenzoic acid (H₃TCM) with Mn²⁺, Cu²⁺, and Co²⁺ salts afforded four interesting metal–organic frameworks (MOFs), [Mn₂(TCM)­Cl­(H₂O)₃]·3DMF·3CH₃OH (<b>1</b>), [Mn₄(TCM)₂(CH₃COO)₂(DMF)₅]·4CH₃OH (<b>2</b>), [Cu₂(TCM)­(CH₃COO)­(DMF)­(H₂O)]·2DMF·3CH₃OH (<b>3</b>) and [Co₃(TCM)₂(H₂O)₅]·5DMF·3CH₃OH (<b>4</b>). Single crystal X-ray diffraction analysis revealed that the four structures based on the flexible TCM tripod consist of honeycomb lattices with different metal–ligand macrocycles. The assembly of the metal–ligand macrocycles and framework topologies is dependent on the coordination geometries of transition metal cations. The two-dimensional coordination network of <b>1</b> was further connected by an auxiliary acetate ligand to give rise to a three-dimensional honeycomb network of <b>2</b>. The TCM ligand centered photoluminescences of these compounds are very sensitive to the coordination modes of the TCM ligands, the metal secondary building units (SBUs), and their microstructures. These MOFs also present interesting magnetic behaviors, as revealed by the study of the magnetic susceptibilities

A Luminescent Mixed-Lanthanide-Organic Framework Sensor for Decoding Different Volatile Organic Molecules

A flexible tripodal polyaromatic acid (4,4′,4″-(((2,4,6-trimethylbenzene-1,3,5-triyl)-tris­(methylene))-tris­(oxy))­tribenzoic acid, H₃TCM) was used to adapt the coordination sites of lanthanide ions for the construction of microporous lanthanide-organic frameworks (LOFs) [LnTCM­(H₂O)₂]·3DMF·H₂O (Ln-TCM; Ln = La, Eu, and/or Tb). In these LOFs, the emission band of TCM matches well with the excitation energy of lanthanide ions (Eu³⁺ and Tb³⁺) which results in high-efficient resonance energy transfer from TCM to lanthanide ions. Moreover, the mixed Eu_<i>x</i>Tb_1–<i>x</i>–TCM has tunable pores to adapt different induced-fit-type host–guest interactions which can modulate both the energy transfer efficiency from TCM to Ln³⁺ ions and the energy allocation between Eu³⁺ and Tb³⁺ ions in the luminescence spectra. We demonstrate that the Eu_<i>x</i>Tb_1–<i>x</i>–TCM sensor has the capability of decoding different volatile organic molecules (VOMs) with a clearly differentiable and unique emission intensity ratio of ⁵D₀ → ⁷F₂ (Eu³⁺, 614 nm) to ⁵D₄ → ⁷F₅ (Tb³⁺, 545 nm) transitions for every different VOM. Compared with the traditional absolute emission intensity method, such a self-referencing emission intensity strategy has generated self-calibrating, highly differentiable, and very stable luminescent signals for decoding different VOMs from the unique Eu_<i>x</i>Tb_1–<i>x</i>–TCM platform, which has great potential for practical applications

A Luminescent Mixed-Lanthanide-Organic Framework Sensor for Decoding Different Volatile Organic Molecules

A flexible tripodal polyaromatic acid (4,4′,4″-(((2,4,6-trimethylbenzene-1,3,5-triyl)-tris­(methylene))-tris­(oxy))­tribenzoic acid, H₃TCM) was used to adapt the coordination sites of lanthanide ions for the construction of microporous lanthanide-organic frameworks (LOFs) [LnTCM­(H₂O)₂]·3DMF·H₂O (Ln-TCM; Ln = La, Eu, and/or Tb). In these LOFs, the emission band of TCM matches well with the excitation energy of lanthanide ions (Eu³⁺ and Tb³⁺) which results in high-efficient resonance energy transfer from TCM to lanthanide ions. Moreover, the mixed Eu_<i>x</i>Tb_1–<i>x</i>–TCM has tunable pores to adapt different induced-fit-type host–guest interactions which can modulate both the energy transfer efficiency from TCM to Ln³⁺ ions and the energy allocation between Eu³⁺ and Tb³⁺ ions in the luminescence spectra. We demonstrate that the Eu_<i>x</i>Tb_1–<i>x</i>–TCM sensor has the capability of decoding different volatile organic molecules (VOMs) with a clearly differentiable and unique emission intensity ratio of ⁵D₀ → ⁷F₂ (Eu³⁺, 614 nm) to ⁵D₄ → ⁷F₅ (Tb³⁺, 545 nm) transitions for every different VOM. Compared with the traditional absolute emission intensity method, such a self-referencing emission intensity strategy has generated self-calibrating, highly differentiable, and very stable luminescent signals for decoding different VOMs from the unique Eu_<i>x</i>Tb_1–<i>x</i>–TCM platform, which has great potential for practical applications

Plasmon-Enhanced C–C Bond Cleavage toward Efficient Ethanol Electrooxidation

Ethanol, as a sustainable biomass fuel, is endowed with the merits of theoretically high energy density and environmental friendliness yet suffers from sluggish kinetics and low selectivity toward the desired complete electrooxidation (C1 pathway). Here, the localized surface plasmon resonance (LSPR) effect is explored as a manipulating knob to boost electrocatalytic ethanol oxidation reaction in alkaline media under ambient conditions by appropriate visible light. Under illumination, Au@Pt nanoparticles with plasmonic core and active shell exhibit concurrently higher activity (from 2.30 to 4.05 A mgPt–1 at 0.8 V vs RHE) and C1 selectivity (from 9 to 38% at 0.8 V). In situ attenuated total reflection–surface enhanced infrared absorption spectroscopy (ATR-SEIRAS) provides a molecular level insight into the LSPR promoted C–C bond cleavage and the subsequent CO oxidation. This work not only extends the methodology hyphenating plasmonic electrocatalysis and in situ surface IR spectroscopy but also presents a promising approach for tuning complex reaction pathways

MiR-338-3p Inhibits Hepatocarcinoma Cells and Sensitizes These Cells to Sorafenib by Targeting Hypoxia-Induced Factor 1α

<div><p>Hypoxia is a common feature of solid tumors and an important contributor to anti-tumor drug resistance. Hypoxia inducible factor-1 (HIF-1) is one of the key mediators of the hypoxia signaling pathway, and was recently proven to be required for sorafenib resistance in hepatocarcinoma (HCC). MicroRNAs have emerged as important posttranslational regulators in HCC. It was reported that miR-338-3p levels are associated with clinical aggressiveness of HCC. However, the roles of miR-338-3p in HCC disease and resistance to its therapeutic drugs are unknown. In this study, we found that miR-338-3p was frequently down-regulated in 14 HCC clinical samples and five cell lines. Overexpression of miR-338-3p inhibited HIF-1α 3′-UTR luciferase activity and HIF-1α protein levels in HepG2, SMMC-7721, and Huh7 cells. miR-338-3p significantly reduced cell viability and induced cell apoptosis of HCC cells. Additionally, HIF-1α overexpression rescued and HIF-1α knock-down abrogated the anti-HCC activity of miR-338-3p. Furthermore, miR-338-3p sensitized HCC cells to sorafenib <i>in vitro</i> and in a HCC subcutaneous nude mice tumor model by inhibiting HIF-1α. Collectively, miR-338-3p inhibits HCC tumor growth and sensitizes HCC cells to sorafenib by down-regulating HIF-1α. Our data indicate that miR-338-3p could be a potential candidate for HCC therapeutics.</p></div

miR-338-3p and sorafenib synergistically inhibited subcutaneous tumor growth.

<p>(A) Representative photos of tumor tissues from different treatment groups 35 days post-injection. (B) Mean tumor volumes measured every seven days. (C) Representative photos of sections stained with an anti-HIF-1α antibody; scale bar 0.15 mm. (D) Average mouse body weight. n = 8 in each group. Data are shown as mean ± SEM.</p

Inhibitory effect of miR-338-3p on HCC cells is mediated by down-regulating HIF-1α.

<p>(A) HIF-1α levels in HepG2 cells transfected with miR-338-3p and/or HIF-1α determined by western blot. (B) Cell viability and (C-D) % apoptotic in HepG2 cells transfected with miR-338-3p and/or HIF-1α plasmid under hypoxic conditions; n = 4. (E) HIF-1α levels in HepG2 cells transfected with miR-338-3p and/or HIF-1A siRNA determined by western blot. (F) Cell viability and (G-H) % apoptotic in HepG2 cells transfected with miR-338-3p and/or HIF-1A siRNA under hypoxia; n = 4. Cell apoptosis was assessed after two days of culture under hypoxic conditions. **p≤0.01 compared to NC group. ## p≤0.01 compared to miR-338-3p only group. Data are shown as mean ± SEM of three independent experiments.</p

miR-338-3p suppresses HIF-1α expression by directly targeting the <i>HIF1A</i> 3′UTR.

<p>(A) Predicted miR-338-3p target sequences in the <i>HIF1A</i> 3′UTR. (B) Western blot analysis of HIF-1α levels in NC- or miR-338-3p-transfected cells. β-actin was used as loading control. Cells were cultured under hypoxia at two days post-transfection with cells cultured under normoxia as reference, and 24 h later protein levels were analyzed. (C) Relative miR-338-3p levels in miR-338-3p mimic transfected HCC cells. Transcript levels were normalized to <i>U6</i> expression. n = 4. (D) Six nucleotides (red) of HIF 3′UTR were mutated to prevent binding with miR-338-3p. (E) Luciferase reporter assay of cells transfected with the wild type (wt) or mutant (mut) <i>HIF1A</i> 3′UTR luciferase reporter plasmid with increasing amounts (20 to 50 nM) of negative control miRNA (NC) or miR-338-3p in HCC cells two days post-transfection; n = 4. **p≤0.01 compared to NC group. Data are shown as mean ± SEM of three independent experiments.</p

miR-338-3p inhibits the HIF pathway.

<p>(A) Effect of miR-338-3p on HIF-1α target genes expression including VEGF, GLUT-1 and MDR1, determined by RT- PCR. HepG2 cells were transfected with 50 µM NC or miR-338-3p for 48 h. RT-PCR was performed 24 h after cells were incubated under hypoxia. n = 3. **p≤0.01 to NC group. (B) Effect of miR-338-3p on VEGF, GLUT-1, and MDR1 expression determined by western blot. (C) Luciferase assay of HepG2 cells co-transfected with the hypoxia response element -luc reporter or control-luc reporter with and increasing doses of NC or miR-338-3p. Cells were incubated under hypoxic conditions for 24 h. Firefly luciferase values were normalized to Renilla luciferase activity; n = 4. Data are shown as mean ± SEM of three independent experiments.</p

Down-regulation of miR-338-3p in human Hepatocarcinoma (HCC) tissues and cell lines.

<p>(A) Real-time PCR analysis of miR-338-3p expression in 15 HCC specimens compared to their pair-matched adjacent non-tumor tissues (NTT). Expression levels were normalized to U6 snRNA and expressed as relative change compared to NTT. (B) Real-time PCR analysis of miR-338-3p expression in the liver cell line L02 and HCC cell lines HepG2, SMMC-7721, BEK-7402, Hep3B, and Huh-7. Expression levels were normalized to U6 snRNA and expressed as relative change compared to L02. Data are shown as mean ± SEM of three independent experiments.</p