2,3 : 6,7-Naphthalenediimide-Based Chiral Triangular Macrocycle: Self-Assembled Helix, Outer π-Surface Directed Co-Assembly and Circularly Polarized Luminescence.

Here, we report the synthesis and self-assembly of a novel chiral 2,3 : 6,7-naphthalenediimide-based triangular macrocycle (NDI-Δ) and its chiroptical properties. The enantiomeric NDI-Δ is synthesized by condensation of (RR) or (SS)-trans-1,2-cyclohexanediamine and 2,3,6,7-naphthalenetetracarboxylic 2,3 : 6,7-dianhydride, in which the chirality of the macrocycles is controlled by the diamine. With the rigid outer π-surface, the macrocycle exhibits unique chiroptical properties and self-assembly modes.

Macroscopic homochiral helicoids self-assembled via screw dislocations.

Chirality is a fundamental property in nature and is widely observed at hierarchical scales from subatomic, molecular, supramolecular to macroscopic and even galaxy. However, the transmission of chirality across different length scales and the expression of homochiral nano/microstructures remain challenging. Herein, we report the formation of macroscopic homochiral helicoids with ten micrometers from enantiomeric pyromellitic diimide-based molecular triangle (PMDI-Δ) and achiral pyrene via a screw dislocation-driven co-self-assembly.

Chiroptical switching in the azobenzene-based self-locked [1]rotaxane by solvent and photoirradiation.

Because of its dynamic reversible nature and simple regulation properties, rotaxane systems provided a good route for the construction of responsive supramolecular chiral materials. Here, we covalently encapsulate the photo-responsive guest molecule azobenzene (Azo) in a chiral macrocycle β-cyclodextrin (β-CD) to prepare self-locked chiral [1]rotaxane [Azo-CD]. On this basis, the self-adaptive conformation of [Azo-CD] was manipulated by solvent and photoirradiation; meanwhile, dual orthogonal regulation of the [1]rotaxane chiroptical switching could also be realized.

Blocking PPARγ interaction facilitates Nur77 interdiction of fatty acid uptake and suppresses breast cancer progression.

Nuclear receptor Nur77 participates in multiple metabolic regulations and plays paradoxical roles in tumorigeneses. Herein, we demonstrated that the knockout of Nur77 stimulated mammary tumor development in two mouse models, which would be reversed by a specific reexpression of Nur77 in mammary tissues. Mechanistically, Nur77 interacted and recruited corepressors, the SWI/SNF complex, to the promoters of and to suppress their transcriptions, which hampered the fatty acid uptake, leading to the inhibition of cell proliferation.

Ectosomal PKM2 Promotes HCC by Inducing Macrophage Differentiation and Remodeling the Tumor Microenvironment.

Tumor-derived extracellular vesicles are important mediators of cell-to-cell communication during tumorigenesis. Here, we demonstrated that hepatocellular carcinoma (HCC)-derived ectosomes remodel the tumor microenvironment to facilitate HCC progression in an ectosomal PKM2-dependent manner. HCC-derived ectosomal PKM2 induced not only metabolic reprogramming in monocytes but also STAT3 phosphorylation in the nucleus to upregulate differentiation-associated transcription factors, leading to monocyte-to-macrophage differentiation and tumor microenvironment remodeling.

Nuclear Receptor Nur77 Facilitates Melanoma Cell Survival under Metabolic Stress by Protecting Fatty Acid Oxidation.

Fatty acid oxidation (FAO) is crucial for cells to overcome metabolic stress by providing ATP and NADPH. However, the mechanism by which FAO is regulated in tumors remains elusive. Here we show that Nur77 is required for the metabolic adaptation of melanoma cells by protecting FAO.