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Given a connected subgraph H of an interconnection network G , the H -structure connectivity κ (G ; H) and the H -substructure connectivity κ s (G ; H) of G are two important measurements for fault tolerance of G. The n -dimensional star graph S n is an attractive interconnection network candidate for multiprocessor systems, and it is (n − 1) -regular. Let n ≥ 4 and 0 ≤ r ≤ n − 1. In this paper, we prove that (i) κ (S n ; K 1 , r) = κ s (S n ; K 1 , r) = n − 1 , and (i i) the removal of any minimum K 1 , r -cut (or, minimum sub- K 1 , r -cut) will split S n into exactly two components, one of which is a singleton, where K 1 , r is a tree on 1 + r vertices, r of which are leaves. The main results generalize some known ones. [ABSTRACT FROM AUTHOR]

Epithelial mesenchymal transition (EMT) is highly correlated with metastasis during cancer development. Although previous studies have revealed that ISO is able to inhibit cancer cell invasion and stem-cell properties, little is known about the effects of ISO on EMT markers. The present study explores the potential regulation of ISO on EMT, leading to the inhibition of migration and invasion of bladder cancer cells. We found that ISO inhibited Vimentin, one of the EMT markers, in the invasive bladder cancer cell lines U5637 and T24T. ISO reduced Vimentin protein level by increasing the expression of METTL14. On the other hand, ISO upregulated the METTL14 mRNA by activating the transcription factor FOXO3a. The results demonstrate that ISO inhibits invasion by affecting the EMT marker and offer a novel insight into understanding the upregulation of METTL14 by ISO. • The effect on EMT and its potential mechanisms of ISO is first explored. • ISO treatment significantly upregulated the protein expression of METTL14 via activating its promoter. • ISO treatment inhibited the Vimentin expression by increasing the expression of METTL14. • The study of the effect on anti-cancer by ISO provides novel insight against BC. [ABSTRACT FROM AUTHOR]

Muscle invasive bladder cancer (MIBC) is characterized by a poor overall survival rate in patients. Therefore, innovation and evaluation of idea anti-cancer compounds is of importance for reducing the mortality of MIBCs. The chemotherapeutic activity of ChlA-F, a novel C8 fluoride derivative of cheliensisin A with potent anti-neoplastic properties, was barely investigated. We reported here that ChlA-F treatment significantly induced miR-494 expression and suppressed cell invasion in human MIBC cells. Our results indicated that miR-494 was downregulated in M1 metastatic BC patients in comparison to non-metastatic (M0) BC patients, and such downregulation was also well correlated with over survival rate for MIBC patients. Mechanistically, ChlA-F-induced upregulation of miR-494 was due to a HuR-mediated increase in JunB mRNA stabilization and protein expression, which led to an increase in miR-494 transcription via directly binding to the miR-494 promoter region, while the upregulated miR-494 was able to bind the 3′-UTR region of c-Myc mRNA, resulting in decreased c-Myc mRNA stability and protein expression and further reducing the transcription of c-Myc-regulated MMP-2 and ultimately inhibiting BC invasion. Our results provide the first evidence showing that miR-494 downregulation was closely associated with BC metastatic status and overall BC survival, and ChlA-F was able to reverse the level of miR-494 with a profound inhibition of human BC invasion in human invasive BC cells. Our studies also reveal that ChlA-F is a promising therapeutic compound for BCs and miR-494 could also serve as a promising therapeutic target for the treatment of MIBC patients. • MiR-494 downregulation is closely associated with BC metastatic status and overall BC survival. • ChlA-F treatment significantly induce miR-494 expression and suppressed cell invasion in human MIBC cells. • ChlA-F-induced upregulation of miR-494 is due to a HuR-mediated increase in JunB mRNA stabilization and protein expression. • MiR-494 could also serve as a promising therapeutic target for the treatment of MIBC patients. [ABSTRACT FROM AUTHOR]

ChlA-F is a novel conformation-derivative of Cheliensisin A, styryl-lactone isolates that show potent anti-tumor potential in vivo and vitro. However, the anti-cancer activity and its potential mechanisms underlying ChlA-F action have never been explored. In the present study, we evaluated the potency of ChlA-F on autophagy-mediated anchorage-independent growth inhibition in human high-grade invasive bladder cancer (BC) cells. We found that ChlA-F treatment significantly inhibited anchorage-independent growth of human BC cells by inducing autophagy in a Sestrin-2 (SESN2)-dependent fashion. Our results revealed that ChlA-F treatment specifically induced SESN2 expression via increasing its transcription and mRNA stability. On one hand, ChlA-F treatment markedly attenuated Dicer protein abundance, in turn abolishing miR-27a maturation and further relieving miR-27a binding directly to SESN2 mRNA 3'UTR, thereby promoting SESN2 mRNA stabilization. On the other hand, ChlA-F treatment promoted Sp1 abundance and consequently mediated SESN2 transcription. These results demonstrate that its activation of the autophagic pathway through specifically promoting SESN2 expression mediates the anti-cancer effect of ChlA-F, which offers insights into the novel anti-cancer effect of ChlA-F on BC, as well as providing therapeutic alternatives against human BC. [ABSTRACT FROM AUTHOR]

Abstract: Three novel lanthanum chloride–erythritol complexes (LaCl3·C4H10O4·5H2O (LaE(I)), LaCl3·C4H10O4·3H2O (LaE(II)), and LaCl3·1.5C4H10O4 (LaE(III)) were synthesized and characterized by single crystal X-ray diffraction, FTIR, far-IR, THz, and Raman spectroscopy. The coordination number of La3+ is nine. LaE(I) and LaE(II) have similar coordination spheres, but their hydrogen bond networks are different. Erythritol exhibits two coordination modes: two bidentate ligands and tridentate ligands in LaE(III). Chloride ions and water coordinate with La3+ or participate in the hydrogen-bond networks in the three complexes. Crystal structures, FTIR, FIR, THz, and Raman spectra provide detailed information on the structures and coordination of hydroxyl groups to metal ions in the metal–carbohydrate complexes. [Copyright &y& Elsevier]

Abstract: Two complexes of neutral d-galactitol (C6H14O6, G) with terbium nitrate, TbGN(I) and TbGN(II), and one complex with samarium nitrate SmGN were synthesized and characterized. From IR, FIR, THz and luminescence spectra the possible coordinations were suggested, and the single-crystal X-ray diffraction results confirm the spectroscopic conclusions. In TbGN(I) (Tb(NO3)3·C6H14O6·3H2O), the Tb3+ is 9-coordinated with three water molecules and six OH groups from two d-galactitol molecules. Nitrate ions do not coordinate to metal ions, which is different from other reported lanthanide nitrate–d-galactitol complexes. In TbGN(II) and SmGN (Ln(NO3)3·C6H14O6), Ln3+ is 10-coordinated with six OH groups from two d-galactitol molecules and four oxygen from two bidentate nitrate ions, and one nitrate ion is hydrogen bonded. No water exists in the structures. d-Galactitol molecules provide their 1-, 2- and 3-hydroxyl groups to coordinate with one metal ion and their 4-, 5- and 6-hydroxyl groups to coordinate with another metal ion in the three structures. There is still a new topological structure that can be observed for lanthanide–d-galactitol complexes, which indicates that the coordinations between hydroxyl groups and metal ions are complicated. [Copyright &y& Elsevier]

Abstract: The interactions between metal ions and hydroxyl groups of carbohydrates are important for their possible biological activities. Here two HoCl3–galactitol complexes ([Ho(galac)(H2O)3)]Cl3·0.5galac) (HoG(I)) and ([Ho2(galac)(H2O)12)]Cl6·2H2O) (HoG(II))) and one ErCl3–galactitol complex ([Er(galac)(H2O)3)]Cl3·0.5galac)(ErG)) were prepared and characterized. The possible structures of HoG(I) and ErG were deduced from FTIR, elemental analysis, ESI-MS, FIR, THz and TGA results. It is suggested that Ho3+ or Er3+ is 9-coordinated with six hydroxyl groups from two galactitol molecules and three water molecules, and another galactitol molecule is hydrogen-bonded in HoG(I) and ErG and the ratio of metal to ligand is 1:1.5. The structure of HoG(II) was determined by FTIR and X-ray diffraction analyses. The results demonstrate that lanthanide ions with galactitol may form two compounds in a system and different topological structures can be obtained. [Copyright &y& Elsevier]

Recent studies show p85α up-regulates epidermal growth factor (EGF) receptor, thereby promoting malignant cell transformation and migration in normal mouse embryonic fibroblasts (MEFs). However, the potential role of p85α in human bladder cancer (BC) remains unknown. Here, we show that p85α is down-regulated in BC tumor tissues. Ectopic expression of p85α inhibited cell invasion, but not migration, whereas p85α knockdown promoted invasion in BC cells, revealing that p85α inhibits BC invasion. Overexpression of kinase-deficient p110 in T24 T(p85α) cells inhibited BC cell migration, but not invasion, suggesting that the inhibition of p85α on invasion is independent of PI3K activity. The effect of p85α on inhibiting BC invasion was mediated by the inactivation of MMP-2 concomitant with the up-regulation of TIMP-2 and down-regulation of MMP-14. Mechanistic studies revealed c-Jun inactivation was associated with p85α knockdown-induced MMP-14 expression, and down-regulated miR-190, leading to ATG7 mRNA degradation. This suppressed the autophagy-dependent removal of TIMP-2 in human BC cells. The present results identify a novel function of p85α and clarify the mechanisms underlying its inhibition of BC invasion, providing insight into the role of p85α in normal and cancer cells. [ABSTRACT FROM AUTHOR]