Theranostic Rhenium(I)-Based ER-Phagy Retardant Promotes Immunogenic Cell Death.

ER-phagy is a double-edged sword in the occurrence, development, and treatment of cancer; especially, its functions in immunotherapy are still unknown. In this work, we designed a theranostic Re complex () containing a BODIPY-derived ligand and a β-carboline ligand to target the endoplasmic reticulum (ER) and block ER-phagy at the late stages. Interestingly, as validated both in vitro and in vivo, ER-phagy blockage greatly enhances the capability of to induce immunogenic cell death (ICD).

Identification of mitochondrial ATP synthase as the cellular target of Ru-polypyridyl--carboline complexes by affinity-based protein profiling.

Ruthenium polypyridyl complexes are promising anticancer candidates, while their cellular targets have rarely been identified, which limits their clinical application. Herein, we design a series of Ru(II) polypyridyl complexes containing bioactive β-carboline derivatives as ligands for anticancer evaluation, among which shows suitable lipophilicity, high aqueous solubility, relatively high anticancer activity and cancer cell selectivity. The subsequent utilization of a photo-clickable probe, , serves to validate the significance of ATP synthase as a crucial target for through photoaffinity-based protein profiling.

Pt(IV)-Deferasirox Prodrug Combats DNA Damage Repair by Regulating RNA N-Methyladenosine Methylation.

DNA damage repair is considered to be an important mechanism of cisplatin resistance, and the roles of iron homeostasis in action mechanisms of cisplatin have not been studied yet. Herein, a Pt(IV) prodrug () integrating cisplatin and the clinical oral iron-chelating agent deferasirox () is found to be highly active toward cisplatin-insensitive triple-negative breast cancer cells both and . RNA-sequencing shows that can downregulate genes related to the double-strand break (DSB) damage pathway significantly.

Self-Amplifying Iridium(III) Photosensitizer for Ferroptosis-Mediated Immunotherapy Against Transferrin Receptor-Overexpressing Cancer.

Photoimmunotherapy is attractive for cancer treatment due to its spatial controllability and sustained responses. This work presents a ferrocene-containing Ir(III) photosensitizer (IrFc1) that can bind with transferrin and be transported into triple-negative breast cancer (TNBC) cells via a transferrin receptor-mediated pathway. When the ferrocene in IrFc1 is oxidized by reactive oxygen species, its capability to photosensitize both type I (electron transfer) and type II (energy transfer) pathways is activated through a self-amplifying process.

Ru(II)-modified TiO nanoparticles for hypoxia-adaptive photo-immunotherapy of oral squamous cell carcinoma.

The alternations in the hypoxic and immune microenvironment are closely related to the therapeutic effect and prognosis of oral squamous cell carcinoma (OSCC). Herein, a new nanocomposite, TiO@Ru@siRNA is constructed from a ruthenium-based photosensitizer (Ru) modified-TiO nanoparticles (NPs) loaded with siRNA of hypoxia-inducible factor-1α (HIF-1α). Under visible light irradiation, TiO@Ru@siRNA can elicit both Type I and Type II photodynamic effects, which causes lysosomal damage, HIF-1α gene silencing, and OSCC cell elimination efficiently.

Simultaneous Photoactivation of cGAS-STING Pathway and Pyroptosis by Platinum(II) Triphenylamine Complexes for Cancer Immunotherapy.

Activation of the cyclic GMP-AMP synthase-stimulator of the interferon gene (cGAS-STING) pathway is a potent anticancer immunotherapeutic strategy, and the induction of pyroptosis is a feasible way to stimulate the anticancer immune responses. Herein, two Pt complexes (Pt1 and Pt2) were designed as photoactivators of the cGAS-STING pathway. In response to light irradiation, Pt1 and Pt2 could damage mitochondrial/nuclear DNA and the nuclear envelope to activate the cGAS-STING pathway, and concurrently induce pyroptosis in cancer cells, which evoked an intense anticancer immune response in vitro and in vivo.

Real-time tracking of ER turnover during ERLAD by a rhenium complex via lifetime imaging.

Endoplasmic reticulum (ER) degradation by autophagy (ER-phagy) is a recently revealed selective autophagy pathway that plays important roles in organelle turnover and protein degradation, but the biological functions of ER-phagy are largely unknown. Here, we present an ER-targeting Re(I) tricarbonyl complex (Re-ERLAD) that can accumulate in the ER, induce ER-to-lysosome-associated degradation (ERLAD) upon visible light irradiation, and label ER buds and track their morphological alterations during ER-phagy. The emission of Re-ERLAD is sensitive to viscosity, which is a key parameter reflecting the amount of unfolded protein in the ER.

Ferroptosis-Enhanced Cancer Immunity by a Ferrocene-Appended Iridium(III) Diphosphine Complex.

Ferroptosis is a programmed cell death pathway discovered in recent years, and ferroptosis-inducing agents have great potential as new antitumor candidates. Here, we report a Ir complex (Ir1) containing a ferrocene-modified diphosphine ligand that localizes in lysosomes. Under the acidic environments of lysosomes, Ir1 can effectively catalyze Fenton-like reaction, produce hydroxyl radicals, induce lipid peroxidation, down-regulate glutathione peroxidase 4, and result in ferroptosis.

Moist exposed burn therapy in recovery of patients with immature, red hypertrophic scars successfully treated with a pulsed dye laser in combination with a fractional CO laser.

Background: The efficacy of pulsed dye laser combined (PDL) and UltraPulse fractional CO in treatment of hypertrophic scars is well documented. The present study investigates the efficacy of moist exposed burn ointment (MEBO)/moist exposed burn therapy (MEBT) in postlaser wound management.

Methods: Sixty-one patients with immature, red hypertrophic scars were enrolled in this clinical trial.

Clinical efficacy of utilizing Ultrapulse CO combined with fractional CO laser for the treatment of hypertrophic scars in Asians-A prospective clinical evaluation.

Background And Objective: Hypertrophic scarring is seen regularly. Tissue penetration of laser energy into hypertrophic scars using computer defaults from some lasers may be insufficient and penetration not enough. We have developed a treatment with an interrupted laser "drilling" by the Ultrapulse CO (Manual Fractional Technology, MFT) and, a second pass, with fractional CO .