Search

Dysregulation of the discoidin domain receptors (DDRs) has been implicated in the development of numerous types of tumors, including head and neck cancer, and nasopharyngeal, breast, ovarian and esophageal carcinomas. Furthermore, agents that inhibit DDR1 activity are hypothesized to be useful for the treatment of nasopharyngeal carcinoma (NPC). The aim of the present study was to evaluate the effect of the DDR1 inhibitory (3-(2-(pyrazolo(1,5-a) pyrimidin-6-yl)-ethynyl)benzamide compound, 7RH, in NPC cells both in vitro and in vivo, and its effect when used in combination with dasatinib, a SRC family kinase (SFK) inhibitor. The effects of 7RH alone or in combination with dasatinib on cell viability were assessed using MTT assays and apoptosis was detected by flow cytometry. In addition, western blotting was performed to analyze the relative protein expression levels of cell cycle-associated genes in human NPC cell lines (CNE1, CNE2, HONE1 and SUNE1). Cell migration was also assessed using cell adhesion assays. Furthermore, tumor xenografts of CNE2 NPC cells were established in nude mice and the growth inhibitory effects of 7RH treatment alone or in combination with dasatinib were evaluated. Finally, knockdown of DDR1 protein expression was achieved by transfection of CNE2 cells with DDR1-specific small interfering RNA. Treatment with 7RH effectively suppressed the proliferation and induced the apoptosis of NPC cells. In addition, the Janus kinase 1 (JAK1)/signal transducer and activator of transcription (STAT3) signaling pathway was downregulated by 7RH, whereas the activities of the Ras/Raf/mitogen-activated protein kinase kinase (MEK)/extracellular signal-regulated kinase (ERK) and phosphoinositide 3-kinase (PI3K)/AKT signaling pathways were upregulated in response to 7RH treatment. Furthermore, the expression levels of phosphorylated SRC were increased in NPC cells treated with 7RH; thus indicating that SRC exhibits a vital function in the resistance of NPC cells to 7RH via activation of the PI3K/AKT signaling pathway. The results of the present study indicate that DDR1 and SFK inhibition may present a potential therapeutic strategy for patients with NPC. [ABSTRACT FROM AUTHOR]

By the method of H NMR prescreening and tracing the diagnostic proton signals of the methyl groups, three additional new triquinane-type sesquiterpenoids--chondrosterins K-M (1-3) and the known sesquiterpenoid anhydroarthrosporone (4)--were isolated from the marine fungus Chondrostereum sp. Their structures were elucidated on the basis of MS, 1D, and 2D NMR data. Chondrosterin K is a rare hirsutane sesquiterpenoid, in which a methyl group was migrated from C-2 to C-6 and has a double bond between C-2 and C-3. Compounds 1-3 showed significant cytotoxicities against various cancer cell lines in vitro. [ABSTRACT FROM AUTHOR]

Background: Hepatocellular carcinoma (HCC) is one of the most fatal malignancies worldwide, and CD133 is a popular cancer stem cell (CSC) marker for HCC. CD133(+) CSCs have been reported to resist conventional chemo- and radiotherapy, but little is known about their response to immune surveillance. Interferon-gamma (IFN-γ) is one of key cytokines that the immune system produce to eradicate cancer cells, so we investigated the function of IFN-γ on CD133+ HCC CSCs in this study. Methods: The response of CD133(+) cells to IFN-γ was performed with functional assays (cell proliferation assay and tumor formation in nude mice), flow cytometry, immunofluorescence staining and RNA interference. Results: We found that IFN-γ inhibited the proliferation of cell lines with low percentage of CD133(+) cells (wild-type human cells, BEL7402, QGY7701) but it did not affect the proliferation of cell lines with high percentage of CD133(+) cells (wild-type human cells, Huh7, PLC8024) in vivo and in vitro (nude mice). Flow cytometry analysis demonstrated that the percentage of CD133+ cells increased after IFN-γ treatment of low CD133(+) cell lines. Furthermore, IFN-γ induced the autophagy of low CD133(+) cell lines to decrease proliferation. Conclusion: CD133(+) HCC CSCs resisted IFN-γ-induced autophagy, which might also be a mechanism through which CSCs resist immune eradication. [ABSTRACT FROM AUTHOR]

Heme oxygenase-1 (HMOX-1) is a microsomal enzyme that exerts anti-apoptotic and cytoprotective effects. In the present study, HMOX-1 was demonstrated to be overexpressed and able to be induced by doxorubicin in breast cancer cell lines. Knockdown of HMOX-1 using short interfering (si)RNA enhanced the cytotoxicity of doxorubicin in MDA-MB-231 and BT549 cells. Knockdown of HMOX-1 downregulated B cell lymphoma (Bcl)-2 and Bcl-extra large expression, and significantly enhanced doxorubicin-induced apoptosis in MDA-MB-231 and BT549 cells. Additionally, knockdown of HMOX-1 upregulated light chain 3B expression and markedly increased the accumulation of autophagic vacuoles in MDA-MB-231 and BT549 cells treated with doxorubicin. These results indicated that HMOX-1 may be involved in conferring the chemoresistance of breast cancer cells, by preventing apoptosis and autophagy. Therefore, HMOX-1 may represent a potential therapeutic target for enhancing the cytotoxicity and efficacy of doxorubicin during the treatment of breast cancer. [ABSTRACT FROM AUTHOR]

EBV causes B lymphomas and undifferentiated nasopharyngeal carcinoma (NPC). Although the mechanisms by which EBV infects B lymphocytes have been extensively studied, investigation of the mechanisms by which EBV infects nasopharyngeal epithelial cells (NPECs) has only recently been enabled by the successful growth of B lymphoma Mo-MLV insertion region 1 homolog (BMI1)-immortalized NPECs in vitro and the discovery that neuropilin 1 expression positively affects EBV glycoprotein B (gB)-mediated infection and tyrosine kinase activations in enhancing EBV infection of BMI1-immortalized NPECs. We have now found that even though EBV infected NPECs grown as a monolayer at extremely low efficiency (<3%), close to 30% of NPECs grown as sphere-like cells (SLCs) were infected by EBV. We also identified nonmuscle myosin heavy chain IIA (NMHC-IIA) as another NPEC protein important for efficient EBV infection. EBV gH/gL specifically interacted with NMHC-IIA both in vitro and in vivo. NMHC-IIA densely aggregated on the surface of NPEC SLCs and colocalized with EBV. EBV infection of NPEC SLCs was significantly reduced by NMHC-IIA siRNA knock-down. NMHCIIA antisera also efficiently blocked EBV infection. These data indicate that NMHC-IIA is an important factor for EBV NPEC infection. [ABSTRACT FROM AUTHOR]

Complementary and alternative medicine (CAM) including Japanese Kampo is known to have anticancer potential. An increasing number of cancer survivors are using CAM for disease prevention, immune system enhancement, and symptom control. Although there have been abundant previous clinical reports regarding CAM, scientific investigations aimed at acquiring quantifiable results in clinical trials, as well as basic research regarding CAM, have only recently been undertaken. Recent studies suggest that CAM enhancement of immune function is related to cytokines. This review provides a translational aspect of CAM, particularly Hozai in Kampo from both scientific and clinical points of view for further development of CAM for cancer treatment. [ABSTRACT FROM AUTHOR]

Bioassay-guided fractionation of an ethanol extract of the pericarps of Garcinia mangostana led to the isolation of two new prenylated xanthones, named 1,3,7-trihydroxy-2-(3-methyl-2-butenyl)-8-(3-hydroxy-3-methylbutyl)-xanthone (1) and 1,3,8-trihydroxy-2-(3-methyl-2-butenyl)-4-(3-hydroxy-3-methylbutanoyl)-xanthone (2), together with the five known compounds garcinones C (3) and D (4), gartanin (5), xanthone I (6), and γ-mangostin (7). Their structures were elucidated primarily based on MS and NMR data. Compounds 1-7 showed significant cytotoxic activities against various human cancer cell lines. [ABSTRACT FROM AUTHOR]

Background: Hirsutanol A is a novel sesquiterpene compound purified from fungus Chondrostereum sp. in Sarcophyton tortuosum. Our previous studies had demonstrated that hirsutanol A exhibited potent cytotoxic effect on many kinds of cancer cell lines. In the current study, the antitumor activity of hirsutanol A and its molecular mechanisms were investigated. Methods: Hirsutanol A induced growth inhibition and apoptotic cell death of human colon cancer SW620 cells and human breast cancer MDA-MB-231 cells were determined using MTT assay and flow cytometry assay, respectively. The effect of hirsutanol A on intrinsic ROS level and change in mitochondrial membrane potential (ΔΨm) of different cell lines were also measured by flow cytometry assay. The function of JNK was compromised by JNK siRNA or JNK inhibitor SP600125. The expression of cytochrome c, p-JNK, p-c-Jun after treatment with hirsutanol A were detected by Western blot analysis. Finally, the in vivo anti-tumor effect of hirsutanol A was examined in human cancer cell SW620 xenograft model. Results: The results showed that hirsutanol A significantly induced apoptosis, mitochondrial-independent increase of Reactive Oxygen Species (ROS) level, change of mitochondrial membrane potential, release of cytochrome c in human cancer cells. Preventing increase of ROS level using the potent antioxidant N-acetyl-L-cysteine (NAC) markedly decreased hirsutanol A-induced apoptosis. In addition, JNK signaling pathway was activated by hirsutanol A through elevating ROS level. Blockade of JNK signaling pathway by JNK specific inhibitor SP600125 enhanced apoptosis and hirsutanol A-induced ROS accumulation. Also, hirsutanol A exhibited antitumor activity in human cancer cell SW620 xenograft model. Conclusion: These data suggested that hirsutanol A inhibited tumor growth through triggering ROS production and apoptosis. [ABSTRACT FROM AUTHOR]

Three biflavonoid glycosides along with 12 known flavonoids, were isolated from leaves of Malus hupehensis. The complete structures of two of the compounds were established from analysis of MS, NMR spectroscopic and CD data, as well as DFT CD calculations they were determined to be atropisomeric along a central biaryl axis. The antioxidant activities and protective effects of the compounds against doxorubicin-induced cardiomyopathy in H9c2 cells were also investigated. Amongst all of the isolated compounds, quercetin was the most active radical scavenger with EC50 values of 3.2 μM and 17.8 μM by the DPPH and ABTS∙+ methods, respectively. The results indicated that three of the flavanoids also had a strong protective influence against doxorubicin-induced cell death with EC50 values of 8.3, 5.2 and 7.6 μM, respectively. [ABSTRACT FROM AUTHOR]

Background: To determine the prevalence and risk factors associated with idiopathic epiretinal membranes (iERM) in a Chinese population aged 60 years or older in Beixinjing Blocks, Shanghai. Methods: This population-based study consisted of 3727 participants (89.7% of the eligible). It was performed to describe the prevalence of iERM and possible demographic, systemic, and ocular factors associated with iERM. Each participant underwent a standardized interview and comprehensive ophthalmic examination. iERM was identified and graded from retinal photographs. Then, a case-control study comparing the participants with vs. without iERM was performed to further study the associations between iERM and blood biochemical test results (including fasting plasma glucose, serum creatinine, total cholesterol, and triglyceride), ocular biological parameters (including the axial length, corneal curvature, refractive diopter, intraocular press, and anterior chamber depth), and the data of optical coherence tomography. Results: The prevalence of iERM was 1.02%. iERM was significantly associated with diabetes (OR: 2.457; 95% CI: 1.137, 5.309) and a higher level of education (OR: 1.48; 95% CI: 1.123, 1.952). Blood biochemical test results and ocular biological parameters showed no significant differences between the iERM and control groups, whereas the incidence of posterior vitreous detachment in the iERM group was much higher than in the control group (26.5% vs. 8.8%), but this difference was not statistically significant. Moreover, the eyes with iERM had poorer visual acuity than the eyes without iERM (P<0.05). Conclusions: In Beixinjing Blocks, Shanghai, iERM was relatively rare, was associated with diabetes and a higher level of education, and caused a substantial decrease in visual acuity. [ABSTRACT FROM AUTHOR]

Background: Topotecan produces DNA damage that induces autophagy in cancer cells. In this study, sensitising topotecan to colon cancer cells with different P53 status via modulation of autophagy was examined. Methodology/Principal Findings: The DNA damage induced by topotecan treatment resulted in cytoprotective autophagy in colon cancer cells with wild-type p53. However, in cells with mutant p53 or p53 knockout, treatment with topotecan induced autophagy-associated cell death. In wild-type p53 colon cancer cells, topotecan treatment activated p53, upregulated the expression of sestrin 2, induced the phosphorylation of the AMPKα subunit at Thr172, and inhibited the mTORC1 pathway. Furthermore, the inhibition of autophagy enhanced the anti-tumour effect of topotecan treatment in wild-type p53 colon cancer cells but alleviated the anti-tumour effect of topotecan treatment in p53 knockout cells in vivo. Conclusions/Significance: These results imply that the wild-type p53-dependent induction of cytoprotective autophagy is one of the cellular responses that determines the cellular sensitivity to the DNA-damaging drug topotecan. Therefore, our study provides a potential therapeutic strategy that utilises a combination of DNA-damaging agents and autophagy inhibitors for the treatment of colon cancer with wild-type p53. [ABSTRACT FROM AUTHOR]

Background: A number of published randomized controlled trials have been conducted to evaluate visual performance of blue light-filtering intraocular lenses (IOL) and UV light-filtering intraocular lenses (IOL) after cataract phacoemulsification surgery. However, results have not always been consistent. Therefore, we carried out a meta-analysis to compare the effectiveness of blue light-filtering IOLs versus UV light-filtering IOLs in cataract surgery. Methods and Findings: Comprehensive searches of PubMed, Embase, Cochrane Library and the Chinese BioMedical literature databases were performed using web-based search engines. Fifteen trials (1690 eyes) were included for systematic review, and 11 of 15 studies were included in this meta-analysis. The results showed that there were no significant differences in postoperative mean best corrected visual acuity, contrast sensitivity, overall color vision, or in the blue light spectrum under photopic light conditions between blue light-filtering IOLs and UV light-filtering IOLs [WMD =-0.01, 95%CI (-0.03, 0.01), P = 0.46; WMD= 0.07, 95%CI (-0.04, 0.19), P = 0.20; SMD = 0.14, 95%CI (-0.33, 0.60), P = 0.566; SMD = 0.20, 95%CI (-0.04, 0.43), P = 0.099]. However, color vision with blue light-filtering IOLs was significantly reduced in the blue light spectrum under mesopic light conditions [SMD = 0.74, 95%CI (0.29, 1.18), P = 0.001]. Conclusion: This meta-analysis demonstrates that postoperative visual performance with blue light-filtering IOLs is approximately equal to that of UV light-filtering IOLs after cataract surgery, but color vision with blue light-filtering IOLs demonstrated some compromise in the blue light spectrum under mesopic light conditions. [ABSTRACT FROM AUTHOR]

Diabetic retinopathy (DR) is a major cause of blindness in working age adults, and oxidative stress plays a vital role in the pathogenesis of DR. Pigment-epithelium-derived factor (PEDF), a multifunctional protein, has shown to inhibit the development of DR by accumulating evidence. This paper highlights the current understanding of probable mechanism about how PEDF blocks the deterioration of DR through its antioxidative properties and application prospects of PEDF as a novel therapeutic target in DR. Gene therapy of PEDF is becoming more and more acceptable and will widely be applied to the actual treatment in the near future. [ABSTRACT FROM AUTHOR]

Background: Autophagy is an evolutionarily conserved protein degradation pathway. A defect in autophagy may contribute to tumorigenesis. Autophagy inducers could have a potential function in tumor prevention and treatment. Methodology/Principal Findings: Our results showed that Rhabdastrellic acid-A, an isomalabaricane triterpenoid isolated from the sponge Rhabdastrella globostellata, inhibited proliferation of human cancer cell lines Hep3B and A549 and induced caspase-independent cell death in both the cell lines. Further investigation showed that Rhabdastrellic acid-A induced autophagy of cancer cells determined by YFP-LC3 punctation and increased LC3-II. The pretreatment with autophagy inhibitor 3-MA inhibited Rhabdastrellic acid-A-induced cell death. Knockdown of autophagy-related gene Atg5 inhibited Rhabdastrellic acid-A-induced cell death in A549 cells. Also, phospho-Akt and its downstream targets significantly decreased after treatment with Rhabdastrellic acid-A in both cancer cell lines. Transfection of constitutive active Akt plasmid abrogated autophagy and cell death induced by Rhabdastrellic acid-A. Conclusions/Significance: These results suggest that Rhabdastrellic acid-A could induce autophagy-associated cell death through blocking Akt pathway in cancer cells. It also provides the evidence that Rhabdastrellic acid-A deserves further investigation as a potential anticancer or cancer preventive agent. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the therapeutic efficacy of two surgical procedures used to treat middle thoracic esophageal squamous cell carcinoma and compare the results. A total of 167 patients with middle thoracic esophageal squamous cell carcinoma were included in the study, including 102 patients who underwent Ivor-Lewis esophagectomy and another 65 who underwent dual-incision esophagectomy through the left chest and neck (Dual-incision). The Kaplan–Meier method was used to calculate the survival rate, and Cox regression analysis was performed to identify prognostic risk factors. Perioperative complications occurred in 35 patients (21%). The incidence rate of recurrent laryngeal nerve injury and anastomotic leakage was higher in the Dual-incision group ( p < 0.05), and the incidence rate of gastric retention was higher in the Ivor-Lewis group. However, there were no statistically significant differences. The 3-year local recurrence rate was 37.3% in the Ivor-Lewis group and 40% in the Dual-incision group ( p > 0.05). The overall 5-year survival rate was 34.6%; the rates of the Ivor-Lewis group and the Dual-incision group were 36.0 and 32.3%, respectively ( p > 0.05). The Cox analysis indicated that the pTNM staging was an independent prognostic risk factor ( p = 0.00, hazard ratio = 2.69). Both Ivor-Lewis esophagectomy and Dual-incision esophagectomy through the left chest and neck are options for treating middle thoracic esophageal squamous cell carcinoma. It is suggested that a patient’s individual condition be taken into account when choosing the operative approach. [ABSTRACT FROM AUTHOR]

Background: The oncoprotein Epstain-Barr Virus (EBV)-encoded latent membrane protein1 (LMP1) modulates the pathological effects of the NF-?B, AP-1 and JAK/STAT pathways in nasopharyngeal carcinoma (NPC). Methods: Microarray analysis was performed on the NPC cell line HONE1 stably transfected with a LMP1-expression plasmid or an empty vector. Based on assigned pathways analyzed using the KEGG database, the mTOR signaling pathway was selected for verification by quantitative RT-PCR. Western blot, RNA interference and immunofluorescence were used to determine the relationship between LMP1 and mTOR signing pathway genes, and their clinical significance to NPC. Results: Our studies revealed that overexpression of LMP1 upregulated the mTOR signaling pathway, possibly through phosphorylation of AKT/mTOR/P70S6K/4EBP1 in the NPC cell lines HONE1 and 6-10B. Knockdown of LMP1 reduced expression of p-mTOR and p-4EBP1 in EBV-positive NPC cell line C666-1. In addition, LMP1 expression closely correlated with expression of p-mTOR, p-P70S6K and p-4EBP1 in NPC tumors. Expression of p-P70S6K, p-4EBP1 and LMP1, but not p-mTOR, significantly correlated with overall survival of NPC patients. However, only LMP1 was an independent prognostic factor. Conclusions: These results suggest that the mTOR signaling pathway is regulated by LMP1 expression in NPC. LMP1 and the genes in the mTOR pathway such as p-P70S6K and p-4EBP1 may be potential prognostic biomarkers. [ABSTRACT FROM AUTHOR]

Aim: To determine whether interferon-α (IFNα) can enhance doxorubicin sensitivity in osteosarcoma cells and its molecular mechanism. Methods: Cell viability was evaluated using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Apoptosis was studied using Flow cytometry analysis, Hoechst33258 staining, DNA fragmentation assay, as well as the activation of caspase-3 and poly (ADP-ribose) polymerase. Protein expression was detected by Western blotting. The dependence of p53 was determined using p53-siRNA transfection. Results: IFNα increased doxorubicin-induced cytotoxicity to a much greater degree through apoptosis in human osteosarcoma p53-wild U2OS cells, but not p53-mutant MG63 cells. IFNα markedly upregulated p53, Bax, Mdm2, and p21, downregulated Bcl-2, and activated caspase-3 and PARP cleavage in response to doxorubicin in U2OS cells. Moreover, the siRNA-mediated silencing of p53 significantly reduced the IFNα/doxorubicin combination-induced cytotoxic-ity and PARP cleavage. Conclusion: IFNα enhances the sensitivity of human osteosarcoma U2OS cells to doxorubicin by p53-dependent apoptosis. The proper combination with IFNα and conventional chemotherapeutic agents may be a rational strategy for improving the treatment of osteosarcoma with functional p53. [ABSTRACT FROM AUTHOR]

Krawtchouk polynomials are frequently applied in modern physics. Based on the results which were educed by Li and Wong, the asymptotic expansions of Krawtchouk polynomials are improved by using Airy function, and uniform asymptotic expansions are got. Furthermore, the asymptotic expansions of the zeros for Krawtchouk polynomials are again deduced by using the property of the zeros of Airy function, and their corresponding error bounds are discussed. The obtained results give the asymptotic property of Krawtchouk polynomials with their zeros, which are better than the results educed by Li and Wong. [ABSTRACT FROM AUTHOR]

The study of zeros of orthogonal functions is an important topic. In this paper, by improving the middle variable x(t), we've got a new form of asymptotic approximation, completed with error bounds, it is constructed for the Jacobi functions ϕμ(αβ) (t) (α > -1) as μ → + ∞. Besides, an accurate approximation with error bounds is also constructed correspondingly for the zeros tμ,8 of ϕμ(αβ) (t) (α ≥ -0) as μ → + ∞, uniformly with respect to s = 1,2,.... [ABSTRACT FROM AUTHOR]

The erbB-2 gene encodes tyrosine kinase receptor p185neu. Overexpression of erbB-2 plays a key role in tumorigenesis and the progression of tumors such as breast cancer and ovarian cancer. Our investigation suggests that the anti-inflammatory agent N-(4-ethoxyphenol)-2-hydroxy-acid amide (SUCI02) reversibly represses tyrosine phosphorylation of erbB-2 in a dose-dependent manner, with half maximal inhibition occurring at a concentration of 21.05 µmol/L without reduced erbB-2 receptor expression. Activation of mitogen-activated protein kinase and protein kinase B, downstream molecules of the erbB-2-mediated signal transduction pathway, was inhibited following exposure to SUCI02. In contrast, tyrosine phosphorylation of epidermal growth factor receptor (EGFR) was relatively unaffected by SUCI02. Proliferation of erbB-2-overexpressing BT474 cells was inhibited to a greater extent than proliferation of EGFR-overexpressing A431 cells following exposure to SUCI02. SUCI02 induced cell cycle arrest in G1 phase with upregulation of p27 and downregulation of pRb phosphorylation. Systemic administration of SUCI02 in nude mice resulted in inhibition of erbB-2 tyrosine kinase phosphorylation of subcutaneous human breast cancer BT474 xenografts. We conclude that SUCI02 inhibits erbB-2 tyrosine kinase phosphorylation in vitro and in vivo, shuts down the erbB-2 downstream pathway and induces cell cycle arrest in G1 phase. These results suggest that SUCI02 is a potential novel anticancer agent that deserves further investigation. ( Cancer Sci 2006; 97: 84–89) [ABSTRACT FROM AUTHOR]

A spintronic near-field microwave imaging system without vector network analyzers is used to detect the distribution of microwaves, which are scattered by a sub-wavelength periodical metal wire grating. An ultra thin metal body with diameter of 100 μm (λ/300) is observed by imaging illuminated by a 10 GHz shining source. An application with high sensitivity and resolution detection is proposed in the microwave region under a weak applied external static magnetic field. [ABSTRACT FROM AUTHOR]

The scientific community has witnessed extensive developments and applications of organoboron compounds as synthetic elements and metal-free catalysts for the construction of small molecules, macromolecules, and functional materials over the last two decades. This review highlights the achievements of organoboron-mediated polymerizations in the past several decades alongside the mechanisms underlying these transformations from the standpoint of the polymerization mode. Emphasis is placed on free radical polymerization, Lewis pair polymerization, ionic (cationic and anionic) polymerization, and polyhomologation. Herein, alkylborane/O2 initiating systems mediate the radical polymerization under ambient conditions in a controlled/living manner by careful optimization of the alkylborane structure or additives; when combined with Lewis bases, the selected organoboron compounds can mediate the Lewis pair polymerization of polar monomers; the bicomponent organoboron-based Lewis pairs and bifunctional organoboron-onium catalysts catalyze ring opening (co)polymerization of cyclic monomers (with heteroallenes, such as epoxides, CO2, CO, COS, CS2, episulfides, anhydrides, and isocyanates) with well-defined structures and high reactivities; and organoboranes initiate the polyhomologation of sulfur ylides and arsonium ylides providing functional polyethylene with different topologies. The topological structures of the produced polymers via these organoboronmediated polymerizations are also presented in this review mainly including linear polymers, block copolymers, cyclic polymers, and graft polymers. We hope the summary and understanding of how organoboron compounds mediate polymerizations can inspire chemists to apply these principles in the design of more advanced organoboron compounds, which may be beneficial for the polymer chemistry community and organometallics/organocatalysis community. [ABSTRACT FROM AUTHOR]

Mitotic serine/threonine kinase Aurora-A (Aur-A) plays a critical role in regulating centrosome segregation and spindle assemble. Aur-A overexpression causes excessive centrosome duplication and abnormal spindle structure, leading to tumor malignant progression. Here, we investigated Aur-A expression in nasopharyngeal carcinoma (NPC) and the association between Aur-A and NPC invasiveness. We showed that overexpression of Aur-A in tumor tissues was correlated with cranial bone invasion and clinical stage in NPC patients. Suppression of Aur-A by either selective Aurora inhibitory VX-680 or small-interfering RNA caused G2/M arrest and apoptotic cell death in NPC CNE-2 cells. Significantly, inhibition of Aur-A suppressed CNE-2 cell invasion and restored membrane expression of epithelial markers, E-cadherin and β-catenin, suggesting a reversed epithelial–mesenchymal transition process in cancer cells. In addition, we found that Aur-A-regulated epithelial–mesenchymal transition and invasion were mediated by mitogen-activated protein kinase (MAPK) phosphorylation. Moreover, suppression of MAP kinase by small-interfering RNA or its upstream MEK1/2-selective inhibitor U0126 abrogated cell invasion enhanced by Aur-A overexpression. On the other hand, forced overexpression of constitutively active form of MEK1/2, MEK2DD, in CNE-2 cancer cells rescued cell invasive ability suppressed by VX-680-imposed Aur-A inhibition. Our results indicated that Aur-A acted through a downstream MAP kinase pathway to promote epithelial–mesenchymal transition and invasiveness in nasopharyngeal tumorigenesis. Small chemical inhibitor VX-680 may offer as a promising molecular targeting agent in human NPC. [ABSTRACT FROM AUTHOR]