Dual-Action Therapeutics: DNA Alkylation and Antimicrobial Peptides for Cancer Therapy.

Simple Summary: Conventional cancer treatments, based on chemotherapy and radiotherapy, are often effective but suffer from serious side effects and a potential risk of resistance. Dual therapies, combining DNA alkylating agents and antimicrobial peptides, are generating great interest. Within chemotherapies, a frequently used mechanism is DNA alkylation, inducing DNA damage and subsequent cell death. Antimicrobial peptides, in turn, have demonstrated their efficacy as anticancer agents due to their ability to selectively alter cancer cell membranes. In this review, our aim has been to explore the synergistic potential of these two therapeutic modalities when used together. Cancer remains one of the most difficult diseases to treat, requiring continuous research into innovative therapeutic strategies. Conventional treatments such as chemotherapy and radiotherapy are effective to a certain extent but often have significant side effects and carry the risk of resistance. In recent years, the concept of dual-acting therapeutics has attracted considerable attention, particularly the combination of DNA alkylating agents and antimicrobial peptides. DNA alkylation, a well-known mechanism in cancer therapy, involves the attachment of alkyl groups to DNA, leading to DNA damage and subsequent cell death. Antimicrobial peptides, on the other hand, have been shown to be effective anticancer agents due to their ability to selectively disrupt cancer cell membranes and modulate immune responses. This review aims to explore the synergistic potential of these two therapeutic modalities. It examines their mechanisms of action, current research findings, and the promise they offer to improve the efficacy and specificity of cancer treatments. By combining the cytotoxic power of DNA alkylation with the unique properties of antimicrobial peptides, dual-action therapeutics may offer a new and more effective approach to fighting cancer. [ABSTRACT FROM AUTHOR]