# Synergistic effects of Aurora A and AKT inhibitors combined with radiation in colon cancer cells

## TL;DR

This study shows that combining Aurora A and AKT inhibitors with radiation therapy improves cancer treatment by increasing DNA damage and cell death in colon cancer cells.

## Contribution

The study demonstrates a novel synergistic strategy using Aurora A and AKT inhibitors with radiation to enhance colon cancer treatment.

## Key findings

- Combining Alisertib and MK2206 with radiation significantly reduced cell proliferation and induced G2/M phase arrest.
- The treatment combination increased apoptosis and DNA double-strand breaks in colon cancer cells.
- The synergy of these agents with radiation offers a promising approach to overcome treatment resistance in colon cancer.

## Abstract

This study aimed to investigate the synergistic effects of combining Aurora A and AKT inhibitors with radiation therapy on colon cancer cells and to elucidate the underlying mechanisms. Methods: Human colon cancer cell lines HCT-15 and HCT-116 were treated with Alisertib (Aurora A inhibitor), MK2206 (AKT inhibitor), and radiation alone or in combination. Cell viability, cell cycle distribution, apoptosis, and DNA damage were analyzed using MTT assays, flow cytometry, Western blotting, and immunofluorescence staining, respectively. Results: The combination of Alisertib and MK2206 with radiation significantly suppressed cell proliferation, induced pronounced G2/M phase arrest, and enhanced apoptosis compared to single-agent treatments. Western blot and immunofluorescence analyses revealed elevated γ-H2AX levels, indicating increased DNA double-strand breaks. Conclusion: The integration of Aurora A and AKT inhibitors with radiation therapy synergistically enhances anticancer effects by amplifying DNA damage, disrupting mitotic progression, and inducing apoptosis. This combination represents a promising strategy for overcoming treatment resistance in colon cancer.

The online version contains supplementary material available at 10.1007/s12672-025-02562-8.