Access to Isoquinolines and Isoquinolin-3-ols via Rh(III)-Catalyzed Coupling/Cyclization Cascade Reaction of Arylimidates and Diazo Compounds.

A Rh(III)-catalyzed coupling/cyclization cascade reaction is described, which involves arylimidates and diazo compounds and proceeds via intermolecular C-C bond formation and subsequent intramolecular C-N bond formation. Mechanistic investigation revealed that the reaction is a two-step process: the initial Rh(III)-catalyzed coupling/cyclization proceeds very fast and the following dehydration is rather slow. The reaction provides a direct approach to isoquinolines and isoquinolin-3-ols without any oxidants.

Multicomponent Cascade Synthesis of Trifluoroethyl Isoquinolines from Alkynes and Vinyl Azides.

A multicomponent cascade reaction is described that provides concise access to the trifluoroethyl isoquinolines using a Rh(III)-Cu(II) bimetallic system and readily available Togni's reagent. The system tolerates various vinyl azides and internal alkynes. Experimental results suggest that Togni's reagent might act as a CF3 radical supplier.

Rh(III)-catalyzed C-H activation/cyclization of benzamides and diazo compounds to form isocoumarins and α-pyrones.

Rhodium-catalyzed intermolecular cyclization of benzamides and diazo compounds via C-H activation has been achieved to construct C-C/C-O bonds for the first time. The process provides a facile approach for the construction of isocoumarins and α-pyrones without the need for high temperature or adding oxidants.

DNAJC6 promotes hepatocellular carcinoma progression through induction of epithelial-mesenchymal transition.

Epithelial-mesenchymal transition (EMT) is a developmental program, which is associated with hepatocellular carcinoma (HCC) development and progression. DNAJC6 (DNA/HSP40 homolog subfamily C member 6) encodes auxilin, which is responsible for juvenile Parkinsonism with phenotypic variability. However, the role of DNAJC6 in HCC development and progression is limited. Here, we report that DNAJC6 is up-regulated in HCC tissues and up-regulation of DNAJC6 expression predicts poor outcome in patients with HCC. Furthermore, overexpression of DNAJC6 enhances the ability for acquisition of mesenchymal traits, enhanced cell proliferation and invasion. DNAJC6 positively regulated expression of EMT-related transcription factor, also activating transforming growth factor ß (TGF-ß) pathway to contribute to EMT. Our findings demonstrated an important function of DNAJC6 in the progression of HCC by induction of EMT, and they implicate DNAJC6 as a marker of poor outcome in HCC.