Glutathione S-transferase ω 1 (GSTO1) expression levels have been discovered to be upregulated in various types of cancer. However, to the best of our knowledge, the role of GSTO1 in non-small cell lung cancer (NSCLC) has not been investigated. The present study aimed to investigate the role of GSTO1 in NSCLC and to determine the potential molecular mechanism. GSTO1 expression levels in A549 cells were knocked down using short hairpin RNA and GSTO1 overexpression in H2122 cells was achieved using cDNA constructs. Reverse transcription-quantitative PCR was used to analyze the mRNA expression levels of GSTO1. Cell proliferation was determined using a Cell Counting Kit-8 assay, whereas cell migration and invasion were analyzed using Transwell assays. Flow cytometric analysis was performed to determine the levels of cell apoptosis. The expression levels of GSTO1, Bax, caspase 3, JAK and STAT3 were analyzed using western blotting. The results revealed that GSTO1 overexpression significantly promoted the proliferation, migration and invasion, and inhibited the apoptosis of H2122 cells, whereas the opposite trend was achieved in A549 cells with GSTO1 knockdown. GSTO1 overexpression also significantly increased the phosphorylation levels of JAK and STAT3, whereas the knockdown of GSTO1 promoted the opposite effects. In conclusion, the findings of the present study indicated that GSTO1 may serve as an oncogene in NSCLC. The results suggested that GSTO1 may have an important role in NSCLC by regulating the JAK/STAT3 signaling pathway. Therefore, inhibiting the expression levels of GSTO1 may represent a potential novel therapeutic strategy for NSCLC.

The Ni atom in the title complex, [Ni(SCN)2(C6H14N4)(CH4O)2(H2O)], is six‐coordinate in a slightly distorted octahedral environment. The hexamethylenetetramine ligand binds to the Ni atom through only one of its N atoms, trans to the coordinated water molecule. The thiocyanate and methanol ligands are also mutually trans. In the crystal structure, complex molecules are linked by four different kinds of hydrogen bonds (O—H...S, O—H...N, C—H...N and C—H...O) to form a three‐dimensional network structure.

ABSTRACT:Two acrylic monomers bearing a pyrimidinyl moiety, N-acryloyl-NЈ-2-pyrimidinylpiperazine (APMP) and N-methacryloyl-NЈ-2-pyrimidinylpiperazine (MPMP), are prepared by reactions of N-2-pyrimidinylpiperazine with corresponding acryloyl chlorides in the presence of triethylamine. APMP and MPMP can be polymerized either by using radical initiators such as azobisisobutylonitrile or potassium persulfate (KPS) or by UV light irradiation without any sensitizer. APMP, MPMP, and their polymers are water soluble and liposoluble. They can act as sensitizers to initiate the photopolymerizations of acrylonitrile (AN) in DMF and acrylamide (AAm) or N-acryloylmorpholine (AMPL) in an aqueous medium. They can also act as one component of a redox initiation system by combining with KPS to initiate the polymerization of AAm in an aqueous medium, and a superhigh molecular weight up to 10 6 -10 7 for P(AAm) or 10 5 -10 6 for P(AMPL) is obtained. The above polymerizations are pursued kinetically. The mechanism of the photopolymerizations initiated by MPMP or P(MPMP) are confirmed by an electron spin resonance study. By the fluorescent analysis of PAN and P(AAm) initiated by MPMP, APMP, or their polymers we confirm that they not only initiate the polymerization but also enter the polymer chains. The fluorescence spectra of MPMP, APMP, and their polymers are recorded. A fluorescence structural self-quenching effect is also observed. The fluorescence of P(MPMP) can be quenched by adding electron-deficient unsaturated compounds such as methacrylonitrile, AN, fumaronitrile, tetracyanoethylene, methyl acrylate, and methyl methacrylate and the correlation between the Stern-Volmer constants and the electron deficiency of the quenchers is described. The fluorescence quenching of P(MPMP) by a water-soluble C 60 derivative is also demonstrated.