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C38H29Cl2N4O6.5Pb, triclinic, P1̅ (no. 2), a = 11.548(2) Å, b = 12.532(3) Å, c = 13.661(3) Å, α = 95.34(3)°, β = 112.60(3)°, γ = 103.23(3)°, V = 1740.4 Å3, Z = 2, Rgt(F) = 0.037, wRref(F2) = 0.082, T = 293 K.

Nasopharyngeal carcinoma (NPC) has a high incidence in SoutheastAsia and China. This study aims to investigate the effect of miR-203a-3p and vascular endothelial growth factor-C (VEGF-C) on nasopharyngeal carcinoma. In this study, we investigate the transfection of miR-203a-3p mimics and the ability of miR-203a-3p to inhibit in nasopharyngeal carcinoma cell line 5-8F and C666-1, the expression levels of protein AKT, p-AKT in VEGF-C and the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT) signal pathway by plate clone formation experiment, flow cytometer PI staining method, transwell cell experiment, vasculogenic mimicry experiment, and Western blot. The results showed that miR-203a-3p in the nasopharyngeal carcinoma cell line significantly decreased, while VEGF-C in nasopharyngeal carcinoma tissues and cell lines significantly increased. Furthermore, miR-203a-3p inhibited the proliferation of nasopharyngeal carcinoma cells and blocked the cell cycle of nasopharyngeal carcinoma in the G0 /G1 phase, reduced the vasculogenic phenomena and epithelialmesenchymal transition of nasopharyngeal carcinoma cells, and effectively inhibited the growth of nasopharyngeal carcinoma in vivo. The low expression of VEGF-C can inhibit the proliferation, vasculogenic mimicry, and epithelialmesenchymal transition of nasopharyngeal carcinoma cells. We found that miR-203a-3p was expressed to a low degree in nasopharyngeal carcinoma. Furthermore, miR-203a-3p regulated the PI3K/AKT signal pathway by downregulating the expression of VEGF-C, thereby inhibiting the proliferation, migration, invasion, vasculogenic mimicry, epithelialmesenchymal transition, and other malignant biological characteristics of nasopharyngeal carcinoma cells. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to explore the functional changes of long non-coding ribonucleic acid (lncRNA)-HEIH on hepatocellular carcinoma (HCC) Huh7 and Hep3B cells. PATIENTS AND METHODS: The expression changes of HEIH in 18 pairs of HCC tissues and adjacent normal tissues were detected by quantitative real time-polymerase chain reaction (qRT-PCR). According to its expression changes in HCC cells silenced by short hairpin ribonucleic acid (shRNA) transfection in vitro, these cells were divided into sh-HEIH group and sh-NC group. The effects of lowly expressed HEIH on the proliferation, migration and apoptosis of HCC cells were examined through functional assays. Western blotting was adopted to determine the expression changes of epithelial-mesenchymal transition (EMT) proteins, vimentin, matrix metalloproteinase (MMP)-2 and MMP-3. In addition, the role of HEIH downstream effector micro RNA (miR)-199a-3p in HCC was explored. RESULTS: Compared with adjacent normal tissues, HEIH was highly expressed in HCC tissues (p<0.01). HEIH silencing significantly inhibited the proliferation and migration, but induced the apoptosis of Huh7 cells (p<0.05). The expressions of vimentin and MMP-2 in sh-HEIH group were remarkably lower than those in sh-NC group (p<0.05). Furthermore, miR-199a-3p was identified as the downstream effector of HEIH. The expression of miR-199a-3p increased markedly in Huh7 and Hep3B cells with silenced HEIH expression (p<0.01). Moreover, when miR-199a-3p expression was inhibited, the effects of HEIH on Huh7 and Hep3B cells were weakened, manifested as notably enhanced cell proliferation and migration capabilities (p<0.05). CONCLUSIONS: LncRNA-HEIH suppresses HCC cell growth and metastasis by up-regulating miR-199a-3p. Our findings suggest that HEIH may be a promising target for HCC treatment. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the expression of Stomatin-like protein 2 (SLP-2) and its clinical significance in epithelial ovarian cancer (EOC). PATIENTS AND METHODS: Quantitative real- time polymerase chain reaction (qRT-PCR) was used to detect the differential expression of SLP-2 in EOC tissues and cell lines. The relationship between SLP-2 expression and clinical pathological data of EOC patients was analyzed. RESULTS: QRT-PCR results suggested that the SLP-2 was up-regulated in both EOC tissues and EOC cells by comparing with normal control. SLP-2 expression was a correlation with tumor pathological grade, distant metastasis, and TNM stage in EOC patients. Down-regulation of SLP-2 could significantly inhibit proliferation and promote apoptosis of EOC cells by activating the Notch signaling pathway. Knockdown of SLP-2 markedly downregulated Notch1 and Hes1. CONCLUSIONS: SLP-2 was a novel factor involved in EOC progression, and could be utilized as a potential biomarker and therapeutic target for the EOC patients. [ABSTRACT FROM AUTHOR]

High arsenic (As) groundwater is frequently found in inland basins, yet the contributions of different processes to aqueous As distributions remain unresolved. In the Hetao Basin, a typical inland basin, groundwater As concentrations generally increased from the alluvial fan through the transition area to the flat plain. A geochemical process‐based reactive transport model was established to evaluate and quantify the processes of As mobilization in the northwestern Hetao Basin. Thirty‐six groundwater samples and eight sediment samples were collected from the alluvial fan to the flat plain to investigate the geochemical characteristics of the groundwater system. Along the approximate flow path, groundwater evolved from oxic‐suboxic conditions to anoxic conditions, with increasing concentrations of As, Fe (II), and NH4+, and decreasing Eh and SO4 2−. Modeling results indicated that the observed concentrations of Fe (II) were caused by reductive dissolution of Fe (III) oxides and subsequent precipitation of mackinawite and siderite. Reductive dissolution of Fe (III) oxides was primarily driven by organic matter degradation (>75%), followed by H−S oxidation (<25%). More As was sequestered by mackinawite precipitation and adsorption than that released via abiotic reduction of Fe (III) oxides by H2S oxidation (<25%). More As was sequestered by mackinawite precipitation and adsorption than that released via abiotic reduction of Fe (III) oxides by H2S. Reductive dissolution of Fe (III) oxides was the dominant mechanism for liberating As in both the transition area and the flat plain (>70%), and As desorption under elevated pH and competitive adsorption by HCO3− and PO43− made an important contribution to As enrichment (up to 30%). Overall, this study provides an insight into the relative contributions of different geochemical processes to As enrichment in inland basins. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Parkinson's disease is a neurodegenerative disease that typically results in the loss of dopaminergic neurons, especially in an area of the brain known as the substantia nigra. Here, we investigated the roles of two important neuronal development proteins, dysbindin-1 and SATB2, at different stages of Parkinson's disease. MATERIALS AND METHODS: Using various concentrations of a neurotoxin, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), we established the mouse models at initial and advanced stages of the Parkinson's disease. The pole and rotarod tests were used to assess behavioral response and motor function, respectively. Histology was used to assess the disease pathology. Immunohistochemistry and Western blotting were used to analyze dysbindin-1 and SATB2 expression levels. RESULTS: Compared with controls, the mice in the initial and advanced stages of Parkinson's disease required 2.3-fold and 3.8-fold longer to reach the floor in the pole test. Similarly, in the rotarod test, mice in the initial (168 ± 3.73 s) and advanced stages (91 ± 5.62 s) of Parkinson's disease were less able to maintain motor stability, compared with control mice (214 ± 4.18 s). The expression levels of dysbindin-1 and SATB2 in substantia nigra tissue from control mice were limited but were substantially increased (2.4-fold and 3.6-fold, respectively) in mice in the initial stage of the Parkinson's disease. However, in the mice in the advanced stage of Parkinson's disease, dysbindin-1 expression was 1.7-fold lower, and the SATB2 expression was 1.8-fold higher, than that in the control mice. CONCLUSIONS: The increased expression levels of dysbindin-1 and SATB2 in the initial stage of Parkinson's disease may be due to their protective roles. However, the reduced expression levels in the advanced stage of Parkinson's disease may contribute to irreversible neuronal degeneration. [ABSTRACT FROM AUTHOR]

OBJECTIVE: Cervical cancer is a common tumor in gynecological malignancies. Recent studies showed that long non-coding RNAs (lncRNAs) play a key role in tumorigenesis and development. LncRNA nuclear-rich transcripts 1 (NEAT1) has been found to play a role in gynecological tumors, such as endometrial cancer. However, expression of lncRNA NEAT1 and mechanism in cervical cancer has not been elucidated. MATERIALS AND METHODS: The tumor tissue and adjacent tissue of cervical cancer patients were collected. HeLa cells were cultured in vitro and lncRNA NEAT1 expression was interfered with small interfere RNA (siRNA). Cell proliferation was detected by 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2-H-tetrazolium bromide (MTT) assay. Cell invasion ability was assessed by transwell assay. LncRNA NEAT1, Cyclin D1, and cyclin-dependent kinase 4 (CDK4) expressions were detected by Real-time PCR. Caspase 3 expression was detected by caspase 3 activity kit. Phosphorylated protein kinase B (p-AKT), phosphatidylinositol 3-kinase (p-PI3K), and matrix metalloproteinase-2 (MMP2) levels were evaluated by Western blot. RESULTS: Compared with the adjacent tissue, lncRNA NEAT1 expression was significantly increased in cervical cancer (p<0.05). LncRNA NEAT1 level was decreased in HeLa cells transfected by siRNA, which inhibited the proliferation and invasion of tumor cells, reduced cyclin D1 and CDK4 expressions, enhanced caspase 3 activity, and declined the expressions of p-AKT, p-PI3K, and MMP2 (p<0.05). CONCLUSIONS: LncRNA NEAT1 siRNA transfection can inhibit the proliferation of cervical cancer by regulating the AKT/PI3K signaling pathway, promote cell apoptosis, and restrain cell invasion. Therefore, the lncRNA NEAT1 may be used as a molecular potential for the diagnosis and treatment of cervical cancer through regulating AKT/PI3K signaling pathway, which would be confirmed in the following study. [ABSTRACT FROM AUTHOR]