microRNA-539 functions as a tumor suppressor in papillary thyroid carcinoma via the transforming growth factor ß1/Smads signaling pathway by targeting secretory leukocyte protease inhibitor.

Papillary thyroid carcinoma (PTC) is the most common type of thyroid malignancy, with growing incidence every year. microRNAs (miRs) are known to regulate the physiological and pathological processes of cancers, such as proliferation, migration, invasion, survival, and epithelial-mesenchymal transition (EMT). Herein, this study aimed to investigate the effect of miR-539 on cell proliferation, apoptosis, and EMT by targeting secretory leukocyte protease inhibitor (SLPI) via the transforming growth factor ß1 (TGF-ß1)/Smads signaling pathway in PTC. First, PTC-related differentially expressed genes and regulatory miR were screened using bioinformatics analysis, dual luciferase reporter gene assay, and ribonucleoprotein immunoprecipitation, which identified the SLPI gene and the regulatory miR-539 for this study. We identified SLPI as a highly expressed gene in PTC tissues, and SLPI was targeted and negatively regulated by miR-539. Then, we introduced a series of miR-539 mimics, miR-539 inhibitors, and small interfering RNA against SLPI plasmids into CGTHW-3 cells to examine the effects of miR-539 and SLPI on the expression of TGF-ß1/Smads signaling pathway-, EMT-, and apoptosis-related factors, as well as cell proliferation, migration, invasion, and apoptosis. The obtained results indicated that CGTHW-3 cells treated with silenced SLPI or overexpressed miR-539 suppressed the cell proliferation, migration, invasion abilities, and resistance to apoptosis of PTC cells, corresponding to increased expression of Bcl-2-associated X protein, TGF-ß1, Sekelsky mothers against dpp 4, and epithelial cadherin, and decreased B cell lymphoma 2, Vimentin, and N-cadherin. Altogether, we concluded that overexpressed miR-539 could inhibit the PTC cell proliferation and promote apoptosis and EMT by targeting SPLI via activation of the TGF-ß1/Smads signaling pathway.

Methyl chanofruticosinate type alkaloids from the aerial parts of Kopsia lancibracteolata Merr.

A chemical investigation on the 70% ethanol extract from the leaves and stems of Kopsia lancibracteolata Merr. resulted in the isolation of three new methyl chanofruticosinate type alkaloids, 12-hydroxyl prunifoline A (1), 12-hydroxyl prunifoline C (2), and N(4)-oxide prunifoline D (3). Structural elucidation of all the compounds was performed by spectral methods such as 1D- and 2D-NMR, IR, UV, and HR-ESI-MS. The isolated alkaloids were tested in vitro for cytotoxic potential against five tumor cell lines (BGC-823, HepG2, MCF-7, SGC-7901, and SK-MEL-2). As a result, alkaloid 3 exhibited significant cytotoxic activity against all tested tumor cell lines with IC50 values from 7.2 to 8.9 µM.

catena-Poly[[dichloridozinc(II)]-µ-1,4-bis-(1H-imidazol-1-yl)benzene].

In the title one-dimensional coordination polymer, [ZnCl(2)(C(12)H(10)N(4))](n), the Zn(II) atom (site symmetry 2) is coordinated by two chloride ions and two 1,4-bis-(imidazol-1-yl)benzene ligands, generating a distorted tetra-hedral ZnCl(2)N(2) geometry for the metal ion. The bridging ligand, which is completed by crystallographic inversion symmetry, links the Zn(II) atoms into zigzag chains propagating in [101]. Within the ligand, the dihedral angle between the central benzene ring and terminal imidazole ring is 27.82 (13)°.

2-Fluoro-N'-(2-hy-droxy-benzyl-idene)benzohydrazide.

In the title compound, C(14)H(11)FN(2)O(2), an intra-molecular O-H⋯N hydrogen bond influences the mol-ecular conformation; the two benzene rings form a dihedral angle of 18.4 (3)°. The F atom is disordered over two positions in a 0.717 (5):0.283 (5) ratio. In the crystal, inter-molecular N-H⋯O hydrogen bonds link the mol-ecules into chains extending along the c axis.

2-Fluoro-N'-(2-meth-oxy-benzyl-idene)benzohydrazide.

The mol-ecule of the title compound, C(15)H(13)FN(2)O(2), exists in a trans configuration with respect to the methyl-idene unit. The two benzene rings form a dihedral angle of of 64.7 (2)°. In the crystal, mol-ecules are linked through N-H⋯O hydrogen bonds into chains propagating along the c axis.

MicroRNA-129-5p suppresses nasopharyngeal carcinoma lymphangiogenesis and lymph node metastasis by targeting ZIC2.

PURPOSE: The etiology of nasopharyngeal carcinoma (NPC) is multifactorial, complex and not fully characterized yet. MicroRNAs (miRNAs or miRs) have been found to contribute to the development and progression of NPC. Here, we aimed to investigate the putative role of miR-129-5p in NPC lymphangiogenesis and lymph node metastasis (LNM), including the involvement of its target gene ZIC2 and the Hedgehog signaling pathway. METHODS: The expression of miR-129-5p and ZIC2 in primary NPC tissues was assessed using RT-qPCR and Western blot analyses, followed by LNM and lymph vessel density (LVD) correlation analyses. A direct interaction between miR-129-5p and ZIC2 was verified using a dual-luciferase reporter assay. Gain- and loss-of-function experiments were conducted to investigate the effects of miR-129-5p and ZIC2 expression on NPC cell invasion, migration and proliferation in vitro, as well as on LDV and LNM in nude mice in vivo. Additionally, RT-qPCR and Western blot analyses were performed to determine the expression levels of Hedgehog signaling pathway-related factors. RESULTS: We found that ZIC2 was highly expressed, and miR-129-5p was lowly expressed, in primary NPC tissues. In addition, we found that miR-129-5p can directly bind to and reduce ZIC2 expression. LVD was found to be negatively correlated with miR-129-5p and to be positively correlated with ZIC2 expression. Concomitantly, we found that miR-129-5p abrogated activation of the Hedgehog signaling pathway via ZIC2 targeting, leading to suppression of NPC cell invasion, migration and proliferation in vitro as well as suppression of LNM and LVD in vivo. CONCLUSIONS: From our data we conclude that miR-129-5p, by decreasing ZIC2 expression, may inhibit NPC lymphangiogenesis and LNM through suppression of the Hedgehog signaling pathway.

[Preliminary study on biological characteristics of CD(44)(+) stem cells in human laryngeal carcinoma].

OBJECTIVE: To study the biological characteristics of CD(44)(+) stem cells in human laryngeal carcinoma. METHODS: Tumor samples were obtained from 5 patients, and then the human laryngeal carcinoma cells were cultured in vitro by primary tissue culture technique. Taking CD44 molecule as a marker to isolate CD(44)(+) subpopulation cells from laryngeal carcinoma cells for further study. CD(44)(+) and CD(44)(-) cells were cultured and observed fex their development. CD(44)(+) and CD(44)(-) cells were compared in their functional status (mRNA), cell cycles (G0/G1), their degree of differentiation (CK14 and Involucrin expression) and their morphologic character of the clone. RESULTS: The percentages of CD(44)(+) cells were about 49.8% approximately 53.5% and the median was 51.3%. After culturing CD(44)(+) cells isolated from laryngeal carcinoma could proliferate and the percentage of CD(44)(+) remained the same. CD(44)(+) tumor cells contained much less RNA, more G0/G1 cells, expressed more CK14 protein and less Involucrin protein (less differentiated state). CD(44)(+) cells were multangular in shape with protuberances; CD(44)(-) cells showed a sharp and spindle feature. In comparison with CD(44)(-) cells, CD(44)(+) cells could create heterogeneous offspring by single cell culture of limiting dilution. By observing clone forming rate after single cell planting, it was found that the CD(44)(+) cells had stronger proliferation ability. CONCLUSIONS: CD(44)(+) cells possess some characteristics of stem cells, laryngeal carcinoma stem cells maybe exist in CD(44)(+) cells.