To evaluate the influence of polymorphisms in nucleotide excision repair (NER) and homologous recombination repair (HRR) pathways on the development of osteosarcoma patients.Genotypes of ERCC1 rs11615 and rs3212986, ERCC2 rs1799793 and rs13181, NBN rs709816 and rs1805794, RAD51 rs1801320, rs1801321 and rs12593359, and XRCC3 rs861539 were conducted by Polymerase Chain Reaction Restriction Fragment Length Polymorphism (PCR-RFLP) assay.Total 148 osteosarcoma patients and 296 control subjects were collected from Taizhou First People's Hospital. Conditional logistic regression analyses found that individuals carrying with GA+AA genotype of ERCC2 rs1799793 and GC+CC genotype of NBN rs1805794 were significantly associated with increased risk of osteosarcoma, and the ORs(95%CI) were 1.58(1.03-2.41) and 2.66(1.73-4.08), respectively. We found that GA+AA genotype of ERCC2 rs1799793 or GC+CC genotype of NBN rs1805794 were associated with an increased risk of osteosarcoma in females, with ORs(95%CI) of 2.42(1.20-4.87) and 2.01(1.07-4.23), respectively.Our results suggest that ERCC2 rs1799793 and NBN rs1805794 polymorphisms were associated with an increased risk for osteosarcoma, which suggests that NER and HRR pathways modulate the risk of developing osteosarcoma.
IN THE TITLE COMPOUND [SYSTEMATIC NAME: 1(2),1(5)-dibromo-5(2),5(5)-dimethoxy-2,7-dithia-1,5(1,4)-dibenzenaoctaphane], C(18)H(18)Br(2)O(2)S(2), the dihedral angle between the aromatic rings is 0.6 (2)° and their centroid separation is 3.251 (2) Å, indicating that a trans-annular π-π interaction occurs. The dimeth-oxy and dibromo substituents are located at crossed positions because of the electronic and the steric nature of the substituents.
An entry from the Cambridge Structural Database, the world’s repository for small molecule crystal structures. The entry contains experimental data from a crystal diffraction study. The deposited dataset for this entry is freely available from the CCDC and typically includes 3D coordinates, cell parameters, space group, experimental conditions and quality measures.
Osteosarcoma (OS) is a highly invasive primary malignancy of the bone that is common in children and adolescents. MicroRNAs (miRNAs) are novel diagnostic and predictive biomarkers for cancers. The miRNA miR-3195 is aberrantly expressed in multiple types of tumors. However, the expression levels and biological functions of miR-3195 in OS remain unclear.Two Gene Expression Omnibus (GEO) datasets (GSE69470 and GSE16088) were used to analyze differentially expressed miRNAs and mRNAs in osteosarcoma cell lines and OS tissues. Quantitative RT-PCR was used to detect the expression levels of miR-3195 and the SRY-box transcription factor 4 (SOX4) mRNA in OS tissues and cell lines. The relationship between miR-3195 and the 3'-upstream region (3'-UTR) in the SOX4 mRNA (predicted through bioinformatics) was analyzed using Pearson's correlation analysis and confirmed by a dual-luciferase reporter gene experiment. Cell counting kit-8 assays, colony formation assays, flow cytometry, wound healing assays, transwell assays, and western blotting were performed to explore the effects of miR-3195 levels on SOX4 affected OS cell biological behavior.Our results revealed that miR-3195 was the most down-regulated miRNA and SOX4 was the most up-regulated mRNA by Bioinformatic analysis. It was further confirmed miR-3195 had low expression, and SOX4 had high expression levels in clinical OS tissue samples; the expression levels of both genes were negatively correlated with each other in OS tissues. Overexpression of miR-3195 in OS cell lines significantly inhibited cell proliferation, migration, and invasiveness, while promoting apoptosis; all these effects were reversed by increasing SOX4 expression levels. We also found that miR-3195 could directly bind with the SOX4 gene and down-regulate SOX4 expression.miR-3195 can modulate proliferation, migration, invasiveness, and apoptosis in OS cells by regulating the SOX4 gene. Thus, the miR-3195/SOX4 signaling may be a novel therapeutic target in OS treatment.
A series of dialkyne building blocks based on the dithia[3.3]paracyclophane unit have been synthesized in good yields. The electronic properties of these novel dialkynes can be tuned through a transannular substitution effect. These synthetically more accessible diethynyldithia[3.3]paracyclophanes are promising candidates for the building of relatively carbon rich molecular scaffolds.
Two dithia[3.3]paracyclophane-bridged bimetallic ruthenium acetylide complexes 2 and 3, in which the upper deck of the cyclophanes were assembled with naphthalenyl and anthracenyl rings, have been designed and synthesized. X-ray crystal structures of 2 and 3 show that there are effective transannular π–π interactions between the two rings in the cyclophane unit. Electrochemistry studies revealed that the successive introduction of naphthalenyl and anthracenyl rings reduced the thermodynamic stability of the corresponding mixed-valence states of 2 and 3. Radical cations and dications of complexes 2 and 3 were generated after the addition of 1.0 or 2.0 equivalents of ferrocenium hexafluorophosphate ([FcH][PF6]). The ν(CC) of radicals 2+++ and 3++ shift 86 nm and 88 nm in contrast to 2 and 3, respectively. UV-Vis-NIR spectra of 2+++ and 3++ exhibited three enveloped transitions in the NIR (10 000–4000 cm−1) range. DFT studies showed that the compositions of the FMOs of 2 and 3 are more naphthalenyl and anthracenyl in character than the upper deck of complex 1. Spectroscopy and DFT studies indicated that the influence of transannular π–π interactions on the electronic transitions is more pronounced than in complex 1.
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