<b>BACKGROUNDb>S100A8 and S100A9 are two members of the S100 protein family characterized by the presence of two Ca2+-binding sites of the EF-hand type. Previous studies suggested that the whole S100 family displays significant functions in tumor growth, progression and invasion. This study aimed to determine the expression of the two indices of the family, S100A8 and S100A9, in lung cancer tissues and normal lung tissues and its correlation with clinical features.

<b>METHODSb>A total of 60 cases with a variety of clinical data that were diagnosed with different histological subtypes of lung cancer were investigated. Semi-quantitative reverse transcriptase-PCR (Sq-Rt-PCR) and immunohistochemical staining of cancer, adjacent and peripheral lung tissues were executed to distinguish the expression patterns of S100A8 and S100A9 and to further clarify their correlation with clinical features.

<b>RESULTSb>Immunohistochemical staining of both proteins showed a significant up-regulation in lung cancer tissue (S100A8, S100A9, P<0.0001), and PCR revealed that the levels of S100A8 and S100A9 expression were significantly higher in lung cancer tissues (S100A8 P=0.002/0.004; S100A9 P=0.022/0.026). The higher expression was found to be correlated with the clinical characteristics of adenocarcinoma, inflammation and stage IV lesion.

<b>CONCLUSIONSb>S100A8, S100A9 up-regulation was found in the lung adenocarcinoma and end stage lung cancer tissue, the correlation of which with their higher expression in inflammatory lung tissues may indicate the collaborative effect of inflammation on the progression of cancer.

Adenocarcinoma ; genetics ; metabolism ; pathology ; Aged ; Calgranulin A ; genetics ; metabolism ; Calgranulin B ; genetics ; metabolism ; Female ; Humans ; Immunohistochemistry ; Inflammation ; genetics ; metabolism ; pathology ; Lung Neoplasms ; genetics ; metabolism ; pathology ; Male ; Middle Aged ; Reverse Transcriptase Polymerase Chain Reaction

OBJECTIVE: To investigate the effect of methylation transferase inhibitor 5-aza-2'-deoxycitydine (5-aza-2 dC) on the growth, differentiation and apoptosis of human acute myeloid leukemia(AML) cell line HL-60, and to explore the possible anti-leukemia mechanism of 5-aza-2 dC. METHODS: HL-60 cells were treated by 5-aza-2 dC at various concentrations for different periods of time. The effect of 5-aza-2 dC on the growth of HL-60 cells were detected by MTT assay. The effect on the cell cycle and differentiation were detected by flow cytometry. The effect on the apoptosis were detected by Hochest33342 staining and flow cytometry. The expression of S100A8 and S100A9 was detected by reverse transcription-polymerase chain reaction (RT-PCR). RESULTS: (1) 5-aza-2 dC inhibited the growth of HL-60 cells in a concentration- and time-dependent manner, and HL-60 cells were arrested at G2/M phases; (2) 5-aza-2 dC enhanced the expression of cell differentiation antigen CD11b at HL-60 cells, especially at the low drug concentration; (3) 5-aza-2 dC induced HL-60 cell apoptosis in a concentration- and time-dependent manner, especially at the high drug concentration; (4) 5-aza-2 dC increased the expression levels of S100A8 and S100A9 mRNA in HL-60 cells. CONCLUSION 5-aza-2 dC can inhibit the growth of HL-60 cells accompanied with G2/M phase arrest, induce the differentiation and apoptosis of the cells, and increase the expression levels of S100A8 and S100A9 mRNA, which may be the anti-AML mechanism of 5-aza-2 dC.
Antimetabolites, Antineoplastic ; pharmacology ; Apoptosis ; drug effects ; Azacitidine ; analogs & derivatives ; pharmacology ; Calgranulin A ; biosynthesis ; genetics ; Calgranulin B ; biosynthesis ; genetics ; Cell Proliferation ; drug effects ; Cell Transformation, Neoplastic ; drug effects ; Decitabine ; HL-60 Cells ; Humans ; RNA, Messenger ; biosynthesis ; genetics

<b>OBJECTIVEb>To investigate the expression of myeloid-related protein complex (MRP-8/14) in children with acute Kawasaki Disease (KD).

<b>METHODSb>A total of 41 children with acute KD and 40 age- and sex-matched control children with upper respiratory tract infection were recruited. Serum levels of MRP-8/MRP-14 complex were measured by ELISA, messenger ribonucleic acid (mRNA) abundance of MRP-8 and MRP-14 in circulating granulocytes and monocytes was determined by RT-PCR, and the number of circulating endothelial cells was determined by flow cytometry.

<b>RESULTSb>When the analysis was stratified according to the presence or absence of coronary artery ectasia in the KD patient group, serum levels of MRP-8/MRP-14 complex, MRP-8 and MRP-14 mRNA abundance in granulocytes, and the number of circulating endothelial cells were all significantly higher in KD patients with coronary artery ectasia than in KD patients without coronary artery ectasia (P<0.05). Serum levels of MRP-8/MRP-14 complex were positively correlated with the number of endothelial cells in the circulation (r=0.69, P<0.05).

<b>CONCLUSIONSb>Serum levels of MRP-8/MRP-14 complex are elevated in a positive association with the number of circulating endothelial cells in KD children with coronary artery ectasia, suggesting a causative role in the development of coronary artery lesions.

Acute Disease ; Calgranulin A ; blood ; genetics ; physiology ; Calgranulin B ; blood ; genetics ; physiology ; Child, Preschool ; Coronary Artery Disease ; etiology ; Endothelial Cells ; pathology ; Female ; Humans ; Infant ; Male ; Mucocutaneous Lymph Node Syndrome ; blood ; complications ; pathology ; RNA, Messenger ; analysis

S100 calcium binding protein A9 (S100A9) is involved in a variety of biological processes such as inflammation and tumor cell migration and invasion regulation. The purpose of this study was to construct S100A9 gene-edited mice by using CRISPR/Cas9 technology, thereby providing an animal model for exploring the biological functions of this gene. According to the S100A9 gene sequence, the single-stranded small guide RNA (sgRNA) targeting exons 2 and 3 was transcribed in vitro, and a mixture of Cas9 mRNA and candidate sgRNA was injected into mouse fertilized eggs by microinjection. Early embryos were obtained and transferred to surrogate mice, and F
Animals ; Bronchoalveolar Lavage Fluid ; CRISPR-Cas Systems/genetics* ; Calgranulin B ; Disease Models, Animal ; Gene Knockout Techniques ; Gene Targeting ; Lung ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Ovalbumin ; Phenotype

<b>OBJECTIVEb>To explore mechanism of S100A8 in the oncogenesis and development of laryngeal cancer.

<b>METHODSb>Proteins interacting with S100A8 were isolated from laryngeal cancer cell lines Hep-2 by immunoprecipitation assay with anti-S100A8 antibody. The target bands were cut out and identified by maxtrix assisted laser desorption/ionization time of flight (MALDI-TOF). The peptide mass fingerprinting data of the proteins identified were analyzed based on the Mascot database. The NF-kappa B binding sites of the proteins were predicted by P-Match software. The binding ability of one of the proteins to S100A8 was confirmed by co-immunoprecipitation and immunocytochemistry methods.

<b>RESULTSb>Four proteins interacting with S100A8 were obtained, which were hypothetical protein LOC80154, MHC class I HLA-B, similar to T-box 1 isoform C and sarcolemmal associated protein 1. The four genes were predicted to have NF-kappa B binding sites. MHC class I HLA-B, which is one of targets in NF-kappa B pathway, was first confirmed to have the binding ability to S100A8.

<b>CONCLUSIONb>The novel partners of S100A8 identified in the study might be involved in NF-kappa B pathway. The binding ability of MHC class I HLA-B to S100A8 implies that S100A8 might function as a new member with other proteins including HLA-B in NF-kappa B pathway. These findings provide a new clue to further study on the molecular mechanism of S100A8 in the genesis of laryngeal carcinomas.

Animals ; Binding Sites ; Calgranulin A ; genetics ; metabolism ; Carcinoma, Squamous Cell ; genetics ; metabolism ; pathology ; Cell Line, Tumor ; HLA-B Antigens ; genetics ; metabolism ; Humans ; Laryngeal Neoplasms ; genetics ; metabolism ; pathology ; NF-kappa B ; metabolism ; Signal Transduction

The potential use of urinary nucleic acids as diagnostic markers in prostate cancer (PCa) was evaluated. Ninety-five urine samples and 234 prostate tissue samples from patients with PCa and benign prostatic hyperplasia (BPH) were analyzed. Micro-array analysis was used to identify candidate genes, which were verified by the two-gene expression ratio and validated in tissue mRNA and urinary nucleic acid cohorts. Real-time quantitative polymerase chain reaction (qPCR) was used to measure urinary nucleic acid levels and tissue mRNA expression. The TSPAN13-to-S100A9 ratio was selected to determine the diagnostic value of urinary nucleic acids in PCa (P = 0.037) and shown to be significantly higher in PCa than in BPH in the mRNA and nucleic acid cohort analyses (P < 0.001 and P = 0.013, respectively). Receiver operating characteristic (ROC) analysis showed that the area under the ROC curve was 0.898 and 0.676 in tissue mRNA cohort and urinary nucleic acid cohort, respectively. The TSPAN13-to-S100A9 ratio showed a strong potential as a diagnostic marker for PCa. The present results suggest that the analysis of urine supernatant can be used as a simple diagnostic method for PCa that can be adapted to the clinical setting in the future.
Aged ; Aged, 80 and over ; Biomarkers, Tumor/*genetics/*urine ; Calgranulin B/*genetics ; Cohort Studies ; Humans ; Male ; Middle Aged ; Nucleic Acids/*genetics/*urine ; Oligonucleotide Array Sequence Analysis ; Prostate/metabolism ; Prostatic Hyperplasia/diagnosis/genetics/urine ; Prostatic Neoplasms/diagnosis/*genetics/*urine ; RNA, Messenger/genetics/metabolism ; RNA, Neoplasm/genetics/metabolism ; ROC Curve ; Real-Time Polymerase Chain Reaction ; Tetraspanins/*genetics