Interferon-α stimulates DExH-box helicase 58 to prevent hepatocyte ferroptosis.

BACKGROUND: Liver ischemia/reperfusion (I/R) injury is usually caused by hepatic inflow occlusion during liver surgery, and is frequently observed during war wounds and trauma. Hepatocyte ferroptosis plays a critical role in liver I/R injury, however, it remains unclear whether this process is controlled or regulated by members of the DEAD/DExH-box helicase (DDX/DHX) family. METHODS: The expression of DDX/DHX family members during liver I/R injury was screened using transcriptome analysis. Hepatocyte-specific Dhx58 knockout mice were constructed, and a partial liver I/R operation was performed. Single-cell RNA sequencing (scRNA-seq) in the liver post I/R suggested enhanced ferroptosis by Dhx58hep-/-. The mRNAs and proteins associated with DExH-box helicase 58 (DHX58) were screened using RNA immunoprecipitation-sequencing (RIP-seq) and IP-mass spectrometry (IP-MS). RESULTS: Excessive production of reactive oxygen species (ROS) decreased the expression of the IFN-stimulated gene Dhx58 in hepatocytes and promoted hepatic ferroptosis, while treatment using IFN-α increased DHX58 expression and prevented ferroptosis during liver I/R injury. Mechanistically, DHX58 with RNA-binding activity constitutively associates with the mRNA of glutathione peroxidase 4 (GPX4), a central ferroptosis suppressor, and recruits the m6A reader YT521-B homology domain containing 2 (YTHDC2) to promote the translation of Gpx4 mRNA in an m6A-dependent manner, thus enhancing GPX4 protein levels and preventing hepatic ferroptosis. CONCLUSIONS: This study provides mechanistic evidence that IFN-α stimulates DHX58 to promote the translation of m6A-modified Gpx4 mRNA, suggesting the potential clinical application of IFN-α in the prevention of hepatic ferroptosis during liver I/R injury.

Downregulation of ACE2 is associated with advanced pathological features and poor prognosis in clear cell renal cell carcinoma.

Aims: The aim of this study was to explore the alteration in ACE2 expression and correlation between ACE2 expression and immune infiltration in clear cell renal cell carcinoma (ccRCC). Methods: The authors first analyzed the expression profiles and prognostic value of ACE2 in ccRCC patients using The Cancer Genome Atlas public database. The authors used ESTIMATE and CIBERSORT algorithms to analyze the correlation between ACE2 expression and tumor microenvironment in ccRCC samples. Results: ACE2 was correlated with sex, distant metastasis, clinical stage, tumor T stage and histological grade. Moreover, downregulation of ACE2 was correlated with unfavorable prognosis. In addition, ACE2 expression was associated with different immune cell subtypes. Conclusion: The authors' analyses suggest that ACE2 plays an important role in the development and progression of ccRCC and may serve as a potential prognostic biomarker in ccRCC patients.

Lay abstract To date, the morbidity and mortality of clear cell renal cell carcinoma (ccRCC) are gradually increasing, and ccRCC is more aggressive than other kidney cancer types. The ACE2 protein could alter other protein activity and promote cancer progression. In this study, the authors used publicly available databases, analyzed the ACE2 expression patterns in ccRCC cells and evaluated the link between the presence of ACE2 and the ability of immune cells to enter tumors. Finally, the authors conducted further analyses to explore the mechanism by which ACE2 may be involved in ccRCC cancer progression. The authors found that the presence and activity of ACE2 were low in advanced ccRCC and that this was linked to worse overall survival.

WDR5a functions in cadmium-inhibited root meristem growth by regulating nitric oxide accumulation in Arabidopsis.

MAIN CONCLUSION: Cadmium stress induces WDR5a expression to promote NO accumulation to repress root meristem growth via suppressing auxin transport and synthesis in Arabidopsis. Nitric oxide (NO) synthase (NOS)-like activity plays a vital role in toxic cadmium (Cd)-induced NO production and inhibition of root meristem growth, while factor(s) regulating NOS-like activity and root meristem growth in plant response to Cd has not been identified yet. Here, we report that WD40 repeat 5a (WDR5a) functions in Cd-induced NOS-like activity, NO accumulation and root meristem growth suppression. We found that wdr5a-1 mutant root has increased root meristem growth with lower NOS-like activity and NO accumulation than wild type upon Cd exposure, and exogenous NO donors sodium nitroprusside or nitrosoglutathione can restore its reduced Cd sensitivity. In addition, Cd activates WDR5a expression in roots, and overexpressing WDR5a results in increased NO accumulation and suppressed root meristem growth similar to Cd-stressed wild-type roots, while scavenging NO or inhibiting NOS-like activity significantly reverts these effects of Cd. Furthermore, WDR5a acts in Cd-repressed auxin accumulation through reducing the levels of auxin efflux carriers PIN1/3/7 and biosynthetic enzyme TAA1, and reduced sensitivity of wdr5a-1 root meristem to Cd can be partially reverted by inhibiting TAA1 activity pharmaceutically or mutating TAA1 genetically. This study identified WDR5a as a key factor modulating NO accumulation and root meristem growth in plant response to Cd.

MYCT1 inhibits the EMT and migration of laryngeal cancer cells via the SP1/miR-629-3p/ESRP2 pathway.

MYCT1 has an inhibitory effect on the migration of laryngeal cancer cells, although the underlying molecular mechanism remains unknown. In this study, we aimed to explore the mechanism of MYCT1 in the epithelial-mesenchymal transition (EMT) and migration of laryngeal cancer cells. We found that MYCT1 significantly decreased the expression of miR-629-3p but increased the expression of ESRP2 in laryngeal cancer cells. The expression of miR-629-3p and ESRP2 in laryngeal cancer tissues showed significantly positive and negative correlations with patient metastasis, respectively. miR-629-3p was confirmed to repress the expression of ESRP2 by targeting its 3'UTR. SP1 was verified to be a direct transcription factor for miR-629-3p and a downstream target of MYCT1. Moreover, MYCT1 inhibited the EMT and migration of laryngeal cancer cells through the SP1/miR-629-3p/ESRP2 pathway. Taken together, our results establish a novel MYCT1 signaling pathway in the EMT and migration of laryngeal cancer cells, thus providing important insights for further studying the pathway in the diagnosis and treatment of laryngeal cancer.

MYCT1 Inhibits the Adhesion and Migration of Laryngeal Cancer Cells Potentially Through Repressing Collagen VI.

MYCT1, a target of c-Myc, inhibits laryngeal cancer cell migration, but the underlying mechanism remains unclear. In the study, we detected differentially expressed genes (DEGs) from laryngeal cancer cells transfected by MYCT1 using RNA-seq (GSE123275). DEGs from head and neck squamous cell carcinoma (HNSCC) were first screened by comparison of transcription data from the Gene Expression Omnibus (GSE6631) and the Cancer Genome Atlas (TCGA) datasets using weighted gene co-expression network analysis (WGCNA). GO and KEGG pathway analysis explained the functions of the DEGs. The DEGs overlapped between GSE6631and TCGA datasets were then compared with ours to find the key DEGs downstream of MYCT1 related to the adhesion and migration of laryngeal cancer cells. qRT-PCR and Western blot were applied to validate gene expression at mRNA and protein levels, respectively. Finally, the cell adhesion, migration, and wound healing assays were to check cell adhesion and migration abilities, respectively. As results, 39 overlapping genes were enriched in the GSE6631 and TCGA datasets, and most of them revealed adhesion function. Thirteen of 39 genes including COL6 members COL6A1, COL6A2, and COL6A3 were overlapped in GSE6631, TCGA, and GSE123275 datasets. Similar to our RNA-seq results, we confirmed that COL6 is a target of MYCT1 in laryngeal cancer cells. We also found that MYCT1 inhibited the adhesion and migration of laryngeal cancer cells via COL6. These indicate that COL6 is a potential target of MYCT1 and participates the adhesion and migration of laryngeal cancer cells, which provides an important clue for further study on how MYCT1 regulating COL6 in laryngeal cancer progression.

Downregulation of microRNA-9 reduces inflammatory response and fibroblast proliferation in mice with idiopathic pulmonary fibrosis through the ANO1-mediated TGF-ß-Smad3 pathway.

Idiopathic pulmonary fibrosis (IPF) is a progressive interstitial lung disease with increasing occurrence, high death rates and unfavorable treatment regimens. In the current study, we identified the expression of microRNA-9 (miR-9) and anoctamin-1 (ANO1) in IPF mouse models induced by bleomycin, and their effects on inflammation and fibroblast proliferation through the transforming growth factor-ß (TGF-ß)-Smad3 pathway. To verify the targeting relationship between miR-9 and ANO1, we used bioinformatics prediction and conducted a dual-luciferase reporter gene assay. The underlying regulatory mechanisms of miR-9 and the target gene ANO1 were investigated mainly with the treatment of miR-9 mimic, miR-9 inhibitor, or siRNA against ANO1 in fibroblasts isolated from IPF mice. Enzyme-linked immunosorbent assay was performed to investigate the effect of miR-9 or ANO1 on inflammatory factors. 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and flow cytometry were used to detect fibroblast proliferation and apoptosis. Reverse transcription quantitative polymerase chain reaction and western blot analysis were applied to measure the expression of the TGF-ß-Smad3 pathway-related genes. The determination of luciferase activity suggested that miR-9 targets ANO1. Upregulation of miR-9 or silencing of ANO1 intensified inflammation in IPF, promoted proliferation and inhibited apoptotic ability of lung fibroblasts. MiR-9 negatively modulated ANO1, and thus activated the TGF-ß-Smad3 pathway. These findings suggest that miR-9 can indirectly activate the TGF-ß-Smad3 pathway by inhibiting the expression of ANO1, thereby aggravating inflammation, promotes proliferation and suppressing apoptosis of lung fibroblasts in mice models of IPF.

MiR-140 Expression Regulates Cell Proliferation and Targets PD-L1 in NSCLC.

BACKGROUND/AIMS: Programmed death ligand1(PD-L1) plays a role in the development and progression of non-small cell lung cancer (NSCLC). This study aimed to identify miRNA(s) that are responsible for regulation of expression of PD-L1 in NSCLC, and to investigate the role of PD-L1 in regulation of the cell cycle in NSCLC. METHODS: We predicted the target miRNA of PD-L1, which was miR-140, using the online tools TargetScan and miBase. In NSCLC cells obtained from clinical specimens, in addition to A549 and NCI-H1650 cell cultures, western blots were used to detect the level of expression of proteins, while real-time PCR was used to determine the level of expression of PD-L1, miR-140, cyclin E, and ß-actin. Transfection with miR-140 mimics, miR-140 inhibitors, and PD-L1 siRNA were conducted using commercial kits. To determine whether miR-140 directly binds PD-L1, a luciferase reporter gene with wild type or mutated PD-L1 was used. Cell viability was measured with the MTT assay, and PI staining was used for cell cycle analysis. RESULTS: We found low expression of miR-140 and high expression of PD-L1 and cyclin E in NSCLC cells. Over-expression of miR-140 suppressed the expression of PD-L1 by directly binding its 3' UTR, and was also associated with decreased expression of cyclin E and inhibition of cellular proliferation in A549 and NCI-H1650 cells. Inhibition of PD-L1, in the absence of manipulations to miR-140, also decreased the expression of cyclin E. CONCLUSION: We conclude that miR-140 directly suppresses PD-L1 and inhibits the miR-140/PD-L1/cyclin E pathway in NSCLC.

CREB promotes laryngeal cancer cell migration via MYCT1/NAT10 axis.

PURPOSE: CREB, MYCY1 and NAT10 are involved in cancer cell migration. However, the relationship between these three proteins and their role in laryngeal cancer cell migration remains unknown. METHODS: Transient gene transfection was performed in laryngeal cancer cells. Bioinformatics analysis was used to predict the binding of CREB to MYCT1 promoter. Binding of CREB to the promoter of MYCT1 was monitored by luciferase reporter assay and chromatin immuno-precipitation method in vitro and in vivo, respectively. Real-time RT-PCR and Western bolt were applied to detect gene transcription and translation levels, respectively. Laryngeal cancer cell migration was assayed by transwell chamber experiment. RESULTS: CREB protein expression was significantly up-regulated in laryngeal cancer tissues and associated with cancer differentiation, tumor stage, and lymphatic metastasis. CREB inhibits MYCT1 expression by direct binding to its promoter. Meanwhile, MYCT1 has a negative impact on the NAT10 gene expression. Furthermore, CREB promotes NAT10 expression via down-regulating the MYCT1 gene expression. In addition, contrary to MYCT1, CREB and NAT10 enhanced laryngeal cancer cell migration. MYCT1 and NAT10 significantly rescued the effects of CREB and MYCT1 on Hep2 cell migration, respectively. CONCLUSION: CREB promotes laryngeal cancer cell migration via MYCT1/NAT10 axis, suggesting that CREB might be a potential prognostic marker in laryngeal cancer.

Diagnostic value of acid phosphatases (ACP) in differentiating reactive mesothelial cells from cancer cells in the body fluid effusions.

BACKGROUND: The cytological diagnosis of a malignant epithelial tumor, i.e., a cancer cell in the body fluid effusions is usually made by cytomorphological examination alone; however, diagnostic challenges can occur when the cancer cells are rare or cytological atypia is minimal. Morphological similarity between the cancer and the reactive mesothelial cell is the most common problem in establishing a clear diagnosis. The aim of this study is to investigate whether the cocktail acid phosphatases (ACP) special staining will be a useful tumor marker in differentiation of the reactive mesothelial cells from the cancer cells in the body fluid effusions. METHODS: The cocktail ACP special staining was performed on 212 body fluid effusion samples, which included 128 pleural effusions, 69 ascites, and 15 pericardial effusions. RESULTS: The mesothelial cells were cocktail ACP positive in 84 out of 84 benign effusion cases, and the sensitivity and the specificity were 100% for the benign effusions which including pleural effusions, ascites, and pericardial effusions. On the other hand, 122 out of 128 cancer cases were cocktail ACP negative, indicating that the sensitivity of using the cocktail ACP staining to rule out the malignant effusions was 95.3%. Thus, the cocktail ACP staining is an excellent marker with high sensitivity and specificity to distinguish the carcinoma from the reactive mesothelial cells in the body fluid effusions. CONCLUSIONS: Our finding provided a new tool for cytopathologists in diagnosing the body fluid effusion that could impact clinical decision making.

YY1 directly suppresses MYCT1 leading to laryngeal tumorigenesis and progress.

YY1 is a key transcription factor and plays different roles in various cancers. However, role and mechanism of YY1 in laryngeal cancer are still unknown. YY1 and MYCT1 mRNA and protein levels were detected by Real-time RT-PCR and Western Blot methods, respectively. Binding of YY1 to MYCT1 promoter was predicted and confirmed by bioinformatics and chromatin immunoprecipitation assays, respectively. MYCT1 promoter activity was assessed by dual luciferase assay system. Laryngeal cancer cell proliferation, migration, and apoptosis were evaluated by cell viability, colony formation, cell scratch assay, transwell assay, and flow cytometry methods, respectively. YY1 and MYCT1 were upregulated and downregulated at transcriptional level in laryngeal cancer, respectively, which showed a negative correlation between YY1 and MYCT1 expression in laryngeal cancer. Significantly higher expression of YY1 and lower expression of MYCT1 were found in laryngeal cancer tissues of patients with lymphatic metastasis than those without metastasis.YY1 directly bound to MYCT1 promoter region and inhibited its promoter activity. YY1 silence had similar biological functions as MYCT1 overexpression in repressiveness of proliferation and migration, and promotion of apoptosis in laryngeal cancer cells. However, the effects of YY1 silence were recovered by MYCT1 knockdown. YY1 promotes proliferation and migration with suppression of apoptosis via directly inhibiting MYCT1 in laryngeal cancer cells, suggesting that YY1 is a useful target as a potential oncogene in laryngeal cancer development and progression.

Transcriptional suppression of microRNA-27a contributes to laryngeal cancer differentiation via GSK-3ß-involved Wnt/ß-catenin pathway.

miR-27a regulates cell differentiation in a variety of diseases. However, whether and how miR-27a participates in laryngeal cancer cell differentiation remains unknown. Therefore, we explored role and molecular mechanism of miR-27a in laryngeal cancer differentiation in the study. We found that miR-27a expression was inversely correlated with laryngeal cancer differentiation degree based on the clinical pathological diagnosis of each patient. miR-27 asignificantly rescued differentiation and inhibited ß-catenin, LEF1, OCT4 and SOX2 in Wnt/ß-catenin pathway in all-trans-retinoic acid (ATRA)-induced laryngeal cancer cells. Bindings of RARα to miR-27a and miR-27a to GSK-3ß were confirmed by ChIP and Luciferase reporter assays, respectively. In conclusion, miR-27a is a negative regulator in laryngeal cancer differentiation. RARα-mediated miR-27a transcriptional inactivation releases the inhibition of miR-27a on GSK-3ß leading to laryngeal cancer differentiation through GSK-3ß-involved Wnt/ß-catenin pathway, suggesting that miR-27a is a usefully therapeutic target at least in ATRA-induced laryngeal cancer differentiation.

Integrated analysis of long non-coding RNA­associated ceRNA network reveals potential lncRNA biomarkers in human lung adenocarcinoma.

Accumulating evidence has highlighted the important roles of long non-coding RNAs (lncRNAs) acting as competing endogenous RNAs (ceRNAs) in tumor biology. However, the roles of cancer specific lncRNAs in lncRNA-related ceRNA network of lung adenocarcinoma (LUAD) are still unclear. In the present study, the 465 RNA sequencing profiles in LUAD patients were obtained from the cancer genome atlas (TCGA) database, which provides large sample RNA sequencing data free of charge, and 41 cancer specific lncRNAs, 25 miRNAs and 1053 mRNAs (fold change >2, p<0.05) were identified. Then, the lncRNA-miRNA-mRNA ceRNA network of LUAD was constructed with 29 key lncRNAs, 24 miRNAs and 72 mRNAs. Subsequently, we selected these 29 key lncRNAs to analyze their correlation with clinical features, and 21 of them were aberrantly expressed with tumor pathological stage, TNM staging system, lymph node metastasis and patient outcome assessment, respectively. Furthermore, there were 5 lncRNAs (BCRP3, LINC00472, CHIAP2, BMS1P20 and UNQ6494) positively correlated with overall survival (OS, log-rank p<0.05). Finally, 7 cancer specific lncRNAs were randomly selected to verify the expression in 53 newly diagnosed LUAD patients using qRT-PCR. The expression results between TCGA and qRT-PCR were 100% in agreement. The correlation between AFAP1-AS1 and LINC00472 and clinical features were also confirmed. Thus, our results showed the lncRNA expression profiles and we constructed an lncRNA-miRNA-mRNA ceRNA network in LUAD. The present study provides novel insight for better understanding of lncRNA-related ceRNA network in LUAD and facilitates the identification of potential biomarkers for diagnosis and prognosis.

LncRNA-ATB promotes trastuzumab resistance and invasion-metastasis cascade in breast cancer.

Trastuzumab resistance is leading cause of mortality in HER2-positive breast cancers, and the role of TGF-ß-induced epithelial-mesenchymal transition (EMT) in trastuzumab resistance is well established, but the involvement of lncRNAs in trastuzumab resistance is still unknown. Here, we generated trastuzumab-resistant breast cancer cells with increased invasiveness compared with parental cells, and observed robust epithelial-mesenchymal transition (EMT) and consistently elevated TGF-ß signaling in these cells. We identified long noncoding RNA activated by TGF-ß (lnc-ATB) was the most remarkably upregulated lncRNA in TR SKBR-3 cells and the tissues of TR breast cancer patients. We found that lnc-ATB could promote trastuzumab resistance and invasion-metastasis cascade in breast cancer by competitively biding miR-200c, up-regulating ZEB1 and ZNF-217, and then inducing EMT. In addition, we also found that the high level of lnc-ATB was correlated with trastuzumab resistance of breast cancer patients. Thus, these findings suggest that lncRNA-ATB, a mediator of TGF-ß signaling, could predispose breast cancer patients to EMT and trastuzumab resistance.

Association between the XPD/ERCC2 Lys751Gln polymorphism and risk of cancer: evidence from 224 case-control studies.

Genetic variations in the xeroderma pigmentosum group D (XPD) gene may increase cancer susceptibility by affecting the capacity for DNA repair. A lot of studies have reported the association of XPD Lys751Gln polymorphism with risk of cancer, but the results remained controversial. Hence, we performed a systematic review and conducted a meta-analysis to explore association of the XPD Lys751Gln polymorphism with risk of cancer (78,398 cases and 103,178 controls from 224 studies). Overall, a significantly increased cancer risk was found in all genetic models (dominant model: odds ratio (OR) = 1.10, 95% confidence interval (CI) = 1.06-1.14; recessive model: OR = 1.10, 95% CI = 1.05-1.15; homozygous model: OR = 1.14, 95% CI = 1.08-1.21; heterozygous model: OR = 1.09, 95% CI = 1.05-1.12; additive model: OR = 1.08, 95% CI= 1.05-1.11) when all eligible studies were pooled into the meta-analysis. In further stratified and sensitivity analyses, the elevated risk of cancer remained for subgroups of breast cancer, esophageal cancer, hepatocellular cancer, leukemia, lung cancer, and melanoma. In summary, this meta-analysis suggests the XPD Lys751Gln polymorphism is a genetic susceptibility for some cancer types. Moreover, ethnicity, histological type of cancer, and smokers seem to contribute to varying expressions of the Lys751Gln on some cancer risk. In addition, our work also points out the importance of new studies for Lys751Gln association in endometrial cancer and ovarian cancer, where at least some of the covariates responsible for heterogeneity could be controlled, to obtain a more conclusive understanding about the function of the Lys751Gln polymorphism in cancer development.

Application of MMP-7 and MMP-10 in assisting the diagnosis of malignant pleural effusion.

BACKGROUND: Matrix metalloproteinases (MMP) are proteolytic enzymes that are essentially involved in turnover of the extracellular matrix (ECM). The aim was to investigate the diagnostic value of MMP-7 and MMP-10 as tumor markers in pleural effusion (PE) and evaluate the value of combining MMP-7, MMP-10 and carcinoembryonic antigen (CEA) assays as diagnostic aids for malignant cells. MATERIALS AND METHODS: A total of 179 patients with PE (87 malignant and 92 benign) were included in this study. The levels of MMP-7 and MMP-10 were measured using ELISA. RESULTS: Values for MMP-7 and MMP-10 were significantly higher in malignant PE than those in benign PE (P<0.01). Among all variables evaluated, logistic regression found that MMP-7 and MMP-10 were significantly correlated with the presence of malignant disease (P<0.01). Analysis of receiver operating characteristics (ROC) curves showed that the area under the curve of MMP-10 (0.806) was significantly larger than that of MMP-7 (0.771) and CEA (0.789) (P<0.01). With parallel interpretation, the combination of MMP-10 and CEA achieved the higher sensitivity of 94.6%. The combination of MMP-7 and CEA in serial interpretation was able to boost the specificity to 95.7%. The combination of MMP-7, MMP-10 and CEA produced better sensitivity, specificity, PPV and NPV than MMP-7 and MMP-10 alone. CONCLUSION: MMP-7 and MMP-10 in PE may represent helpful adjuncts to conventional diagnostic tools in ruling out malignancy as a probable diagnosis, thus guiding the selection of patients who might benefit from further invasive procedures.

The immune toxicity of titanium dioxide on primary pulmonary alveolar macrophages relies on their surface area and crystal structure.

Surface properties are critical to assess effects of titanium dioxide (TiO2) primary nanoparticles on the immune function of pulmonary alveolar macrophage (PAMs). In this study the immune toxicity of TiO2 primary nanoparticles on PAMs relies on their surface area and crystal structure were determined. The primary PAMs of rats exposed to different sizes and crystal structure of TiO2 particles at different dosages for 24 hrs were evaluated for cytokines, phagocytosis, chemotaxis and surface molecules expression. Nitric oxide (NO) and tumor necrosis factor-alpha (TNF-alpha) level of PAMs significantly increased when exposed to TiO2 primary particles and there were significant association with the exposure total surface area and crystal structure of TiO2 particles in the former. TiO2 particles showed significant inhibiting effects on phagocytotic ability, chemotactic ability, Fc receptors and MHC-II molecular expression of macrophages compared with control. Exposure dosage and crystal structure of TiO2 particles play effects on phagocytotic ability and chemotactic ability of PAMs. These results suggested that TiO2 nanoparticles could induce the release of inflammatory mediators, initiate the inflammation development and inhibit the immune function of PAMs associated with non-specific immunity and specific immunity relies on surface area and crystal structure. NO activity might be a candidate marker indicating the TiO2 exposure burden and cell damage in PAMs.

Bis{2-[(2-benzoyl-hydrazin-1-yl-idene)meth-yl]-6-meth-oxy-phenolato}iron(III) chloride monohydrate.

In the title mononuclear iron(III) complex, [Fe(C(15)H(13)N(2)O(3))(2)]Cl·H(2)O, the Fe(III) atom has a distorted octa-hedral geometry and is six-coordinated by four O atoms and two N atoms from two ligands. In the crystal structure, the complex cations, Cl(-) anions and water mol-ecules are connected into a chain along [100] through N-H⋯O, O-H⋯Cl and N-H⋯Cl hydrogen bonds. Two adjacent chains are linked by O-H⋯O hydrogen bonds.

[Anti-tumor effect and mechanism of Paeonol on the hepatocellular carcinoma cell line Bel-7404].

OBJECTIVE: To investigate the anti-tumor effect of Paeonol (Pae) on the hepatocellular carcinoma cell line Bel-7404 and its molecular mechanisms. METHODS: Hepatocellular carcinoma cell line Bel-7404 was treated by Pae in various concentrations and different time points respectively; and then the cell proliferation was assayed by light microscope, MTT method. DNA agarose gel electrophoresis and TUNEL were used to detect the apoptosis. The expression of PTEN and Akt were examined by RT-PCR and immunocytochemical ABC method. RESULTS: Compared with the control groups Pae obviously increased the inhibitory and apoptosis rate of hepatocellular carcinoma cell line Bel-7404. It also showed a typical apoptotic morphology and DNA depicted a ladder pattern characteristic of the apoptosis, indicating the presence of DNA fragmentation. RT-PCR and immunocytochemical ABC assay showed that Pae could increase the expression of PTEN and decrease the expression of Akt. CONCLUSION: Pae can increase the anti-hepatocellular carcinoma effect, and its mechanism may be the increase of apoptosis-inducing effect which is regulated by phosphatidylinositol-3-kinase.

[Preliminary determination of organic pollutants in agricultural fertilizers].

Organic pollutants such as polycyclic aromatic hydrocarbons (PAHs) in agricultural fertilizers are new problem deserved more study. Eight kinds of organic pollutants including 43 compounds classified as US EPA priority pollutants in twenty one agricultural fertilizers which were universally used in China were determined by Gas chromatography-mass spectrum (GC-MS). Three kinds of organic pollutants including more than 5 compounds were detected in most fertilizers, composing mainly of phthalic acid esters (PAEs), nitrobenzenes (NBs) and polycyclic aromatic hydrocarbons (PAHs). There were 26 compounds detected in at least one fertilizer, five of them especially PAEs detected in most fertilizer and even in all fertilizers. Benzo(a)pyrene, a strongly carcinogenic compound was detected in two fertilizers. Higher concentrations of compounds were determined in those fertilizers such as multifunction compound fertilizers and coated fertilizers.