Ferroptosis-inducing nanomedicine and targeted short peptide for synergistic treatment of hepatocellular carcinoma.

The poor prognosis of hepatocellular carcinoma (HCC) is still an urgent challenge to be solved worldwide. Hence, assembling drugs and targeted short peptides together to construct a novel medicine delivery strategy is crucial for targeted and synergy therapy of HCC. Herein, a high-efficiency nanomedicine delivery strategy has been constructed by combining graphdiyne oxide (GDYO) as a drug-loaded platform, specific peptide (SP94-PEG) as a spear to target HCC cells, sorafenib, doxorubicin-Fe2+ (DOX-Fe2+), and siRNA (SLC7A11-i) as weapons to exert a three-path synergistic attack against HCC cells. In this work, SP94-PEG and GDYO form nanosheets with HCC-targeting properties, the chemotherapeutic drug DOX linked to ferrous ions increases the free iron pool in HCC cells and synergizes with sorafenib to induce cell ferroptosis. As a key gene of ferroptosis, interference with the expression of SLC7A11 makes the ferroptosis effect in HCC cells easier, stronger, and more durable. Through gene interference, drug synergy, and short peptide targeting, the toxic side effects of chemotherapy drugs are reduced. The multifunctional nanomedicine GDYO@SP94/DOX-Fe2+/sorafenib/SLC7A11-i (MNMG) possesses the advantages of strong targeting, good stability, the ability to continuously induce tumor cell ferroptosis and has potential clinical application value, which is different from traditional drugs.

Controlled Growth of 3D Interpenetrated Networks by NiCo2O4 and Graphdiyne for High-Performance Supercapacitor.

In this paper, the 2D all-carbon graphdiyne, which possesses superior 2D strength and high mixed conductivities for both electrons and ions, is used to protect nickel cobalt oxide nanostructures with multidimensions. The in situ grown graphdiyne seamlessly wraps on nanostructures to form 3D interpenetrating networks, leading to significant improvement in the conductivity and avoidance of the structural degradation. The assembled hybrid asymmetric supercapacitor showed a high specific capacitance of 200.9 F g-1 at 1 A g-1 with an energy density of 62.8 Wh kg-1 and a power density of 747.9 W kg-1. The device also showed a preeminent rate capability (86.4% capacitance retention, while the current density was increased from 1 to 20 A g-1) and an ultrastable long-term cycling performance (the capacitance retention is about 97.7% after 10 000 cycles at a high current density of 20 A g-1).

Gas permeation through graphdiyne-based nanoporous membranes.

Nanoporous membranes based on two dimensional materials are predicted to provide highly selective gas transport in combination with extreme permeance. Here we investigate membranes made from multilayer graphdiyne, a graphene-like crystal with a larger unit cell. Despite being nearly a hundred of nanometers thick, the membranes allow fast, Knudsen-type permeation of light gases such as helium and hydrogen whereas heavy noble gases like xenon exhibit strongly suppressed flows. Using isotope and cryogenic temperature measurements, the seemingly conflicting characteristics are explained by a high density of straight-through holes (direct porosity of ∼0.1%), in which heavy atoms are adsorbed on the walls, partially blocking Knudsen flows. Our work offers important insights into intricate transport mechanisms playing a role at nanoscale.

Graphdiyne oxide nanosheets display selective anti-leukemia efficacy against DNMT3A-mutant AML cells.

DNA methyltransferase 3 A (DNMT3A) is the most frequently mutated gene in acute myeloid leukemia (AML). Although chemotherapy agents have improved outcomes for DNMT3A-mutant AML patients, there is still no targeted therapy highlighting the need for further study of how DNMT3A mutations affect AML phenotype. Here, we demonstrate that cell adhesion-related genes are predominantly enriched in DNMT3A-mutant AML cells and identify that graphdiyne oxide (GDYO) display an anti-leukemia effect specifically against these mutated cells. Mechanistically, GDYO directly interacts with integrin ß2 (ITGB2) and c-type mannose receptor (MRC2), which facilitate the attachment and cellular uptake of GDYO. Furthermore, GDYO binds to actin and prevents actin polymerization, thus disrupting the actin cytoskeleton and eventually leading to cell apoptosis. Finally, we validate the in vivo safety and therapeutic potential of GDYO against DNMT3A-mutant AML cells. Collectively, these findings demonstrate that GDYO is an efficient and specific drug candidate against DNMT3A-mutant AML.