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Published on: December 1, 2016
Disassembling a cancer puzzle: Cell junctions and plasma membrane as targets for anticancer therapy
Olga N Shilova1, Evgeny S Shilov2, André Lieber3
1Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry of the Russian Academy of Sciences, Miklukho-Maklaya St., 16/10, Moscow 117997, Russian Federation.
This review explores enhancing anticancer drug delivery by targeting tumor cell junctions and using permeabilization proteins. It suggests novel agents from pathogens to improve drug penetration and intracellular delivery.
Area of Science:
- Oncology
- Molecular Biology
- Drug Delivery
Background:
- Solid tumors often exhibit enhanced permeability and retention (EPR) effect, but drug penetration remains a challenge.
- Improving drug delivery requires strategies like modifying tumor cell-to-cell junctions and utilizing cell membrane permeabilization proteins.
Purpose of the Study:
- To review epithelial cell junctions as targets for combined anticancer therapy.
- To propose novel sources for agents that enhance tumor permeability and intracellular drug delivery.
Main Methods:
- Literature review focusing on epithelial cell junctions and cell membrane permeabilization proteins.
- Analysis of viral and bacterial pathogens as sources of therapeutic agents.
- Evaluation of pore-forming proteins and peptides for cytoplasmic delivery.
Main Results:
- Epithelial cell junctions represent a viable target for improving drug delivery in solid tumors.
- Viral and bacterial pathogens offer potential sources for novel agents to increase tumor permeability.
- Pore-forming proteins and peptides show promise for direct cytoplasmic delivery of anticancer agents.
Conclusions:
- Targeting cell junctions and employing permeabilization proteins are promising strategies to overcome drug delivery limitations in cancer.
- Exploring microbial agents and pore-forming molecules could lead to advanced anticancer therapeutics.
- Further research is needed to address the in vivo application challenges of these agents.
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