Drug-Loaded Nanogel for Efficient Orchestration of Cell Death Pathways by Intramitochondrial Disulfide Polymerization.
Eun Seong ChoiSangpil KimDohyun KimEunshil ChoiJa-Hyoung RyuPublished in: Small (Weinheim an der Bergstrasse, Germany) (2023)
Chemotherapy using a nanoscaled drug delivery system is an effective cancer therapy, but its high drug concentration often causes drug resistance in cancer cells and normal cell damage. Combination therapy involving two or more different cell signaling pathways can be a powerful tool to overcome the limitations of chemotherapy. Herein, this article presents nanogel (NG)-mediated co-delivery of a chemodrug camptothecin (CPT) and mitochondria-targeting monomer (MT monomer) for efficient activation of two modes of the programmed cell death pathway (apoptosis and necroptosis) and synergistic enhancement of cancer therapy. CPT and the monomer are incorporated together into the redox-degradable polymeric NGs for release in response to the intracellular glutathione. The MT monomer is shown to undergo reactive oxygen species (ROS)-triggered disulfide polymerization inside the cancerous mitochondria in cooperation with the chemotherapeutic CPT elevating the intracellular ROS level. The CPT/monomer interconnection in cell death mechanisms for mitochondrial dysfunction and enhanced cell death is evidenced by a series of cell analyses showing ROS generation, mitochondria damage, impacts on (non)cancerous or drug-resistant cells, and cell death modes. The presented work provides beneficial insights for utilizing combination therapy to facilitate a desired cell death mechanism and developing a novel nanosystem for more efficacious cancer treatment.
Keyphrases
- cell death
- cancer therapy
- cell cycle arrest
- combination therapy
- reactive oxygen species
- drug delivery
- drug resistant
- single cell
- molecularly imprinted
- cell therapy
- oxidative stress
- multidrug resistant
- signaling pathway
- stem cells
- induced apoptosis
- radiation therapy
- acinetobacter baumannii
- squamous cell carcinoma
- dna damage
- emergency department
- pi k akt
- high resolution
- rectal cancer
- drug induced
- endoplasmic reticulum