Polychromatic fluorescent MoS2 quantum dots: fabrication and off-on sensing for fluorine ions in water.

Recently, MoS2 quantum dots (QDs) have receive widespread attention as a promising luminescent material. However, so far, little effort has been made on the multicolor emission of MoS2 QDs. Herein, an in situ iodine doping strategy is presented and used to synthesize tunable-photoluminescent (PL) MoS2 QDs. By fine iodine doping, the PL of the MoS2 QDs (I-MoS2 QDs) can be tuned in the range from 423 nm to 529 nm, which exceeds the as-reported emission wavelength range. Studies using controlled experiments and density functional theory (DFT) reveal that the change in electronic state of MoS2 QDs is responsible for the changing PL due to iodine doping. As-synthesized I-MoS2 QDs combined with Fe3+ is developed as a "turn-off-on" fluorescence sensor for F- ions in water. The fluorescence probe has a fine linear response to F- ions in the concentration range of 2.5-80 µM, and the limit of detection is 1.4 µM (S/N = 3).

A New Strategy to Fight Metallodrug Resistance: Mitochondria-Relevant Treatment through Mitophagy to Inhibit Metabolic Adaptations of Cancer Cells.

Metabolic adaptations can help cancer cells to escape from chemotherapeutics, mainly involving autophagy and ATP production. Herein, we report a new rhein-based cyclometalated IrIII complex, Ir-Rhein, that can accurately target mitochondria and effectively inhibit metabolic adaptations. The complex Ir-Rhein induces severe mitochondrial damage and initiates mitophagy to reduce the number of mitochondria and subsequently inhibit both mitochondrial and glycolytic bioenergetics, which eventually leads to ATP starvation death. Moreover, Ir-Rhein can overcome cisplatin resistance. Co-incubation experiment, 3D tumor spheroids experiment and transcriptome analysis reveal that Ir-Rhein shows promising antiproliferation performance for cisplatin-resistant cancer cells with the regulation of platinum resistance-related transporters. To our knowledge, this is a new strategy to overcome metallodrug resistance with a mitochondria-relevant treatment.

Unveiling the anti-cancer mechanism for half-sandwich and cyclometalated Ir(iii)-based complexes with functionalized α-lipoic acid.

Alpha lipoic acid (LA) is a natural compound and coenzyme with sufficient safety information for serving as a promising anticancer agent. To further clarify the mechanism of action (MoA), two Ir(iii) complexes with the functionalized α-lipoic acid (N∧N-LA, N∧N, 2,2-bipyridine derivative), namely Ir1 and Ir2, were synthesized, where Ir1 possessed a half-sandwich structure with the formula [Ir(Cp*)(N∧N-LA)Cl]PF6 (Cp* = 1,2,3,4,5-pentamethyl-cyclopentadiene) and Ir2 possessed the cyclometalated structure with the formula [Ir(C∧N)2(N∧N-LA)]PF6 (C∧N = 2-phenylpyridine). Even though both complexes were constructed based on the same N∧N-LA ligand, Ir1 showed no cytotoxicity (IC50 > 200 µM), which was due to its low lipophilicity for hard penetration into the cancer cells, easy hydrolysis, and reaction with GSH. Ir2 exhibited excellent cytotoxicity (IC50 = 3.43-6.74 µM) toward diverse cancer cell lines in vitro and a promising ability to overcome the cisplatin-resistance in A549R cells. The anticancer mechanism of Ir2 in A549 cells was investigated in detail, and it was found it could localize and accumulate in the lysosomes of A549 cells, induce ROS, arrest the cycle at G0/G1, and lead to cell death by autophagy. Comparison with Ir-NH2 ([Ir(C∧N)2(N∧N-NH2)]PF6) demonstrated that introduction of the LA ligand to Ir2 could highly enhance the cytotoxicity and help to overcome the cisplatin-resistance. This study of the half-sandwich and cyclometalated Ir(iii)-based anticancer agents highlighted the different MoAs toward cancer cells and provided new insights for understanding their structure-property relationships.