Search

A new complex [Pr3NH]+ [Mn(dca)3]− · H2O (dicyanamide = dca−) was synthesized, in which the Mn2+ cations are bridged by end-to-end dca anions to form three-dimensional [Mn(dca)3]nn− networks and tripropylammonium cations reside in the cavities of these networks. The complex has been characterized by single-crystal X-ray diffraction, infrared spectroscopy, elemental analysis, and magnetic measurements. Magnetic susceptibility data indicate ferromagnetic interactions among the MnII ions. [ABSTRACT FROM AUTHOR]

A new multicage compound [(Me)2EtNH][Mn(N3)3] (Me = methyl, Et = ethyl) with a perovskite-related structure has been synthesized. The manganese(II) cations are bridged by end-to-end (EE) azide anions to form three-dimensional cages with the N,N-dimethylethylammonium cations residing in the cavities of the [Mn(N3)3]nn− cages. The compound has been characterized by single-crystal X-ray diffraction, IR spectroscopy, elemental analysis, second-harmonic generation, and magnetic measurements. The second-harmonic generation results support its noncentrosymmetric polar crystal structure. Magnetic susceptibility measurements show antiferromagnetic interactions among the MnII ions. [ABSTRACT FROM AUTHOR]

Our earlier work has shown that the E3 ligase TRIM56 messenger RNA (mRNA) level and vimentin protein expression followed an inverse correlation in ovarian carcinoma patients; however, the regulatory mechanisms underlying TRIM56 expression is unclear. Steady state expression of TRIM56 mRNA expression in the normal ovarian cell line Moody and ovarian cancer cell lines SKOV‐3, A2780, and Caov‐3 were not significantly different; however, TRIM56 protein expression was significantly lower in the ovarian cancer cell lines compared to the Moody cell line. Polysome profiling showed significant increase in translation of TRIM56 messenger RNA in the Moody cells compared to the SKOV‐3 cells. We performed RNA‐affinity pulldown using biotinylated TRIM56 5 'and 3'‐UTR and postnuclear extracts from Moody and SKOV‐3 cells. Whereas no notable difference was observed in affinity pull‐down obtained with the 5'‐UTR, there was obvious difference in protein binding patterns with the 3'‐UTR. Mass spectrometry was used to determine the most differentially binding protein as poly r (c) binding protein 1 (PCBP1). PCBP1 expression and binding to the 3'‐UTR was both higher in SKOV‐3 cells compared to the Moody cells. Silencing of TRIM56 in Moody cells cause an increase in in vitro migration and invasion, and a similar effect was mimicked by overexpression of PCBP1. Conversely, silencing of PCBP1 or overexpression of TRIM56 in SKOV‐3 cells significantly decreased in vitro migration and invasion. In xenograft assays, SKOV‐3 cells stably overexpressing shRNA targeting PCBP1 decreased metastasis, whereas shRNA‐targeting TRIM56 potentiated detection of metastatic lesions, compared to the parental SKOV‐3 cells themselves. Taken together our results reveal a yet undefined posttranscriptional regulatory mechanism underlying low expression of TRIM56 in ovarian cancer. © 2018 IUBMB Life, 71(1):177–182, 2019 [ABSTRACT FROM AUTHOR]