# Peptide-based strategies for overcoming taxol-resistance in cancer therapy – a narrative review

**Authors:** Angelika Długosz-Pokorska, Katarzyna Gach-Janczak

PMC · DOI: 10.1007/s43440-025-00795-6 · 2025-10-20

## TL;DR

This paper reviews how peptides can help overcome resistance to Taxol in cancer therapy by targeting specific mechanisms and improving treatment precision.

## Contribution

The paper highlights novel peptide-based strategies to counter Taxol resistance through targeted modulation of drug efflux, microtubule stabilization, and apoptosis promotion.

## Key findings

- Peptides can modulate drug efflux and restore Taxol effectiveness in multidrug-resistant cancer cells.
- Peptide-nanoparticle combinations improve tumor penetration and reduce side effects.
- Peptides targeting ABCB1, tubulin, and Bcl-2 show promise in overcoming resistance mechanisms.

## Abstract

Taxol (Tx) is widely used in cancer therapy due to its ability to disrupt microtubule dynamics, inhibiting cell division and tumor proliferation. However, multidrug resistance (MDR) mechanisms, including enhanced drug efflux, altered metabolism, mutations in tubulin, and inhibition of apoptosis, challenge its efficacy. Peptide-based therapies have emerged as promising and significant solutions to overcome Tx resistance. These peptides offer high specificity, lower toxicity, and acceptable cell membrane penetration, enhancing precision medicine capabilities. Recent advancements focus on peptides that modulate drug efflux, stabilize microtubules, and promote apoptosis in cancer cells. The ATP synthase (ATP)-binding cassette transporters (ABC) transporter ABCB1, tubulin subunits, and anti-apoptotic proteins such as Bcl-2 show potential in restoring Tx effectiveness against MDR. Combining peptides with nanoparticle delivery systems improves tumor penetration and reduces side effects. Despite challenges like protease degradation and immunogenicity, peptide treatment addresses limitations. Peptide cancer therapies could revolutionize anticancer treatment by providing targeted, less toxic alternatives, especially for MDR. phenotype.

## Linked entities

- **Proteins:** ATP8A2 (ATPase phospholipid transporting 8A2), ABCB1 (ATP binding cassette subfamily B member 1), gammaTub23C (gamma-Tubulin at 23C), BCL2 (BCL2 apoptosis regulator)
- **Chemicals:** Taxol (PubChem CID 36314)

## Full-text entities

- **Diseases:** cancer (MESH:D009369)
- **Chemicals:** taxol (MESH:D017239)

## Figures

3 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12647341/full.md

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Source: https://tomesphere.com/paper/PMC12647341