Comprehensive analysis of PTEN-related ceRNA network revealing the key pathways WDFY3-AS2 - miR-21-5p/miR-221-3p/miR-222-3p - TIMP3 as potential biomarker in tumorigenesis and prognosis of kidney renal clear cell carcinoma.

Kidney renal clear cell carcinoma (KIRC) is one of the most common malignancies, and there is still a lack of effective biomarkers for early detection and prognostic prediction. In here, we compared the characteristics of RNA sequencing data sets of KIRC samples based on the tumor suppressor gene phosphatase and tensin homolog (PTEN). The 1016 long noncoding RNAs, 48 microRNAs (miRNAs), and 2104 messenger RNAs associated with PTEN were identified and these genes were differentially expressed between tumor and paracancerous tissues. The most relevant pathway was found to be WDFY3-AS2 - miR-21-5p/miR-221-3p/miR-222-3p - TIMP3 according to the rules of competing endogenous RNA (ceRNA) regulation. WDFY3-AS2 and TIMP3 expression were positively correlated and reduced in KIRC samples, while miR-21-5p, miR-221-3p, and miR-222-3p were relatively highly expressed. The relatively low expression of WDFY3-AS2 and TIMP3 in KIRC were associated with poor prognosis in KIRC patients, while higher expression of miR-21-5p, miR-221-3p, and miR-222-3p predicted reduced survival (p < 0.05). Univariate and multivariate Cox regression analysis showed that lower expression of WDFY3-AS2 and TIMP3 was significantly related to tumor grade, tumor size, lymph node metastasis, distant metastasis, and TNM stage. The expression of TIMP3 in KIRC tissues was also verified by immunohistochemistry, and the results were consistent with our analytical data. In summary, this study constructed a new model with clinical predictive value and identified the WDFY3-AS2/TIMP3 pathway that was closely associated with the prognosis of KIRC, which could serve as a promising biomarker for the diagnosis and treatment of KIRC.

Molecular-level insights into the immobilization of vapor-phase mercury on Fe/Co/Ni-doped hierarchical molybdenum selenide.

A novel and efficient adsorbent (TM-MoSe2, TM = Fe, Co, Ni) for mercury removal was developed and studied. The adsorption of mercury species (Hg0, HgCl, and HgCl2) and the oxidation of Hg0 by HCl on TM-MoSe2 (001) surface were explored at molecular level by density functional theory (DFT). The results shown that the Hg0 adsorption capacity of MoSe2 was improved by the doping of Fe/Co/Ni, which was also confirmed by experiments. The initial Hg0 removal efficiency of MoSe2-based adsorbents reached 96.4-100.0%. In addition, HgCl was mainly adsorbed on TM-MoSe2 (001) surface in the form of dissociation. The escape of Hg atom from HgCl resulted in the release of Hg0 again. However, HgCl2 could be fixed well on the surface of adsorbent through molecular adsorption or dissociative adsorption. For the oxidation process of Hg0 by HCl, it abided with the Langmuir-Hinshelwood mechanism. In comparison with direct oxidation (Hg → HgCl2), two-step pathway (Hg → HgCl → HgCl2) was an achievable reaction route with lower energy. Furthermore, the Hg → HgCl process was the rate-limiting step of the two-step pathway. The proposed adsorption and oxidation mechanism of mercury species on TM-MoSe2 (001) provide advanced strategies on the development of adsorbents for industrial mercury removal.

[Observation on myeloid origin of neovascular endothelial cells and infiltration of bone marrow-originated inflammatory cells in a murine tumor model].

BACKGROUND & OBJECTIVE: Some studies indicate that endothelial progenitor cells (EPCs) originated from the bone marrow participate in neoplastic angiogenesis, and that bone marrow origin of inflammatory cells potentially contribute to neoplastic invasion, angiogenesis and metastasis. This study was to observe the origin of neovascular endothelial cells and infiltration of bone marrow-originated inflammatory cells in a murine tumor model. METHODS: Healthy C57BL/6 mice were irradiated with 60Co at 8 Gy. Bone marrow cells of green fluorescent protein (GFP) transgenic C57BL/6 mice (donators) were transplanted intravenously into C57BL/6 mice (recipients) via the tail vein 24 h after irradiation. Lewis lung tumor cells were inoculated subcutaneously into recipient mice 2 weeks after transplantation. The xenograft tumors were removed until their diameters reached approximately 1- 2 cm. Subsequently, tumor vessels and inflammatory cells were observed under fluorescent microscopy and detected using immunohistochemistry (IHC). RESULTS: Unsuccessive green fluorescence emitted by neoplastic vascular endothelial cells and inflammatory cells was observed, most of which appeared positive IHC staining. A large number of macrophages were observed inside or adjacent to the necrotic areas of the tumor. A few lymphatic cells were mainly dispersed inside tumor stroma and tumor cells. CONCLUSIONS: Partial endothelial cells of neoplastic neovessels originate from the bone marrow. The murine tumor model could be used as a specific and direct approach to observe bone marrow-originated cells in neoplasms.