Despite the observation of noncovalent interactions between chalcogen atoms in X-ray crystal structures, catalysis that harnesses the power of such chalcogen−chalcogen bonding interactions to produce advanced molecules remains an unresolved problem. Here, we show that a class of extraordinary chalcogenbonding catalysts enables assembly of discrete small molecules including three β-ketoaldehydes and one indole, leading to the construction of N-heterocycles in a highly efficient manner. The strong activation ability of these rationally designed catalysts provides a general solution to the intrinsic limitations of chalcogen bonding catalysis.

The noncovalent S···O bonding interaction is an evolutionary force that has been smartly exploited by nature to modulate the conformational preferences of proteins. The employment of this type of weak noncovalent force to drive chemical reactions is promising yet remains largely elusive. Herein, we describe a dual chalcogen–chalcogen bonding catalysis strategy that the distinct chalcogen atoms simultaneously interact with two chalcogen-based electron donors to give rise to the catalytic activity, thus facilitating chemical reactions. Conventional approaches to the Rauhut–Currier-type reactions require the use of strongly nucleophilic Lewis bases as essential promoters. The implementation of this dual chalcogen–chalcogen bonding catalysis strategy allows the simultaneous Se···O bonding interaction between chalcogen-bonding donors and an enone and an alcohol, enabling the realization of the Rauhut–Currier-type reactions in a distinct way. The further implementation of a consecutive dual Se···O bonding catalysis approach enables the achievement of an initial Rauhut–Currier-type reaction to give an enone product which further undergoes an alcohol-addition induced cyclization reaction. This work demonstrates that the nearly linear chalcogen-bonding interaction can differentiate similar alkyl groups to give rise to regioselectivity. Moreover, the new strategy shows its advantage as it not only enables less reactive substrates working efficiently but tolerates inaccessible substrates using conventional methods.

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The activation of aziridines typically involves the use of strong Lewis acids or transition metals, and methods relying on weak interactions are rare. Herein, we report that cooperative chalcogen bonding interactions in confined sites can activate sulfonyl-protected aziridines. Among the several possible distinct bonding modes, our experiments and computational studies suggest that an activation mode involving the cooperative Se···O and Se···N interactions is in operation. The catalytic reactions between weakly bonded supramolecular species and nonactivated alkenes are considered as unfavorable approaches. However, here we show that the activation of aziridines by cooperative Se···O and Se···N interactions enables the cycloaddition of weakly bonded aziridine-selenide complex with nonactivated alkenes in a catalytic manner. Thus, weak interactions can indeed enable these transformations and are an alternative to methods relying on strong Lewis acids.

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BackgroundAlthough mammary microcalcification is frequently observed and has been associated with poor survival in patients with breast cancer, the genesis of calcification remains unclear. Carbonic anhydrase I (CA1) has been shown to promote calcification by catalysing the hydration of CO2. This study aimed to determine whether CA1 was correlated with microcalcification and with other processes that are involved in breast cancer tumourigenesis.MethodsCA1 expression in breast cancer tissues and blood samples was detected using western blotting, real-time PCR, immunohistochemistry and ELISA. Calcification was induced in the cultured 4T1 cell line originating from mouse breast tumours, using ascorbic acid and β-glycerophosphate. Acetazolamide, a chemical inhibitor of CA1, was also added to the culture to determine the role of CA1 in calcification. The MCF-7 human breast cancer cell line was treated with anti-CA1 siRNA and was assessed using a CCK-8 cell proliferation assay, an annexin V cell apoptosis assay, transwell migration assay and a human breast cancer PCR array. The tag SNP rs725605, which is located in the CA1 locus, was genotyped using TaqMan® genotyping.ResultsIncreased CA1 expression was detected in samples of breast carcinoma tissues and blood obtained from patients with breast cancer. A total of 15.3 % of these blood samples exhibited a 2.1-fold or higher level of CA1 expression, compared to the average level of CA1 expression in samples from healthy controls. Following the induction of calcification of 4T1 cells, both the number of calcium-rich deposits and the expression of CA1 increased, whereas the calcification and CA1 expression were significantly supressed in the presence of acetazolamide. Increased migration and apoptosis were observed in MCF-7 cells that were treated with anti-CA1 siRNA. The PCR array detected up-regulation of the androgen receptor (AR) and down-regulation of X-box binding protein 1 (XBP1) in the treated MCF-7 cells. Significant differences in the allele and genotype frequencies of rs725605 were detected in the cohort of patients with breast cancer but not in other tumours.ConclusionThe results of this study suggested that CA1 is a potential oncogene and that it contributes to abnormal cell calcification, apoptosis and migration in breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s12885-015-1707-x) contains supplementary material, which is available to authorized users.

As noncovalent chalcogen-bonding interaction is comparatively weak, it remains a true challenge to implement chalcogen-bonding catalysis in an efficient manner. We herein show that a chalcogen-bonding catalysis approach to cyanosilylation of a broad range of ketones can be achieved even using as low as parts per million (ppm) level catalyst loading while the reactions were completed within several minutes at room temperature. Considering the nature of weak noncovalent forces, this chalcogen-bonding catalysis approach is remarkable as it can give up to 10 6 /h turnover frequency numbers.

Herein, we describe a new catalysis platform, supramolecular carbon-bonding catalysis, which exploits the highly directional weak interactions between carbon centers of catalysts and electron donors to drive chemical reactions. To demonstrate this catalysis approach, we discovered a class of cyclopropane derivatives incorporated with carbonyl, ester and cyano groups as catalysts which showed general catalysis capability in different types of benchmark reactions. Among these typical examples, a challenging tail-to-head terpene cyclization can be achieved by supramolecular carbon-bonding catalysis. The co-crystal structures of catalyst and electron donors, comparison experiments, and titrations support a catalysis mode of carbon-bonding activation of Lewis basic reactants. Figure 1. Supramolecular carbon-bonding catalysis.