# Resveratrol–Curcumin Hybrid Selectively Induces Chromosomal Abnormalities and Apoptosis in Colon Adenocarcinoma Cells

**Authors:** Mariane Minussi Baptistella, Aléxia Polo Siqueira, Dâmaris Lizia Santos Magalhães, Bruno Zavan, Carolina Sales de Oliveira, Matheus de Freitas Silva, Ellen Tardelli Falleiros Lima, Claúdio Viegas, Bruno Martins Dala-Paula, Ester Siqueira Caixeta, Marisa Ionta, Pollyanna Francielli de Oliveira

PMC · DOI: 10.3390/antiox14111367 · 2025-11-17

## TL;DR

A new hybrid compound shows promise in fighting colon cancer by disrupting cell division and causing cell death.

## Contribution

A novel resveratrol–curcumin hybrid compound is shown to selectively induce chromosomal abnormalities and apoptosis in colon cancer cells.

## Key findings

- PQM-162 exhibits radical scavenging activity and reduces cell viability in HCT-8 cells.
- The compound inhibits cell cycle progression at the G2/M phase and modulates key cell cycle regulators.
- PQM-162 disrupts redox balance and shows antiproliferative effects in colorectal cancer cells.

## Abstract

Colorectal cancer (CRC) therapy frequently relies on chemotherapeutic agents with high cytotoxicity, low selectivity, and suboptimal efficacy. Thus, the search for alternative therapeutic strategies for CRC continues. In the present work, the antitumor potential of a hybrid compound, which contains fragments derived from resveratrol and curcumin, was evaluated. These natural compounds are known by their antioxidant, chemopreventive, and chemotherapeutic properties. Different methodologic approaches were used to investigate cytotoxic, genotoxic, antiproliferative, and antioxidant effects of a hybrid compound, named PQM-162, on HCT-8 colorectal cancer cells. The results showed that PQM-162 displays radical scavenging capacity as demonstrated by DPPH assay. Furthermore, this substance reduced cell viability and inhibited cell cycle progression at G2/M in HCT-8 cells. Antiproliferative activity of PQM-162 was associated with its ability to modulate the expression of critical regulators of G2/M transition and mitosis progression such as PLK1, AURKB, and CDKN1A. Taken together, our data indicate that PQM-162 is a promising antitumor agent due to its disruption of the redox balance in cancer cells and its modulation of the expression of regulators of the cell cycle and mitotic apparatus.

## Linked entities

- **Genes:** PLK1 (polo like kinase 1) [NCBI Gene 5347], AURKB (aurora kinase B) [NCBI Gene 9212], CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026]
- **Chemicals:** resveratrol (PubChem CID 5056), curcumin (PubChem CID 969516)
- **Diseases:** colorectal cancer (MONDO:0005575), CRC (MONDO:0005575)

## Full-text entities

- **Genes:** CDKN1A (cyclin dependent kinase inhibitor 1A) [NCBI Gene 1026] {aka CAP20, CDKN1, CIP1, MDA-6, P21, SDI1}, AURKB (aurora kinase B) [NCBI Gene 9212] {aka AIK2, AIM-1, AIM1, ARK-2, ARK2, AurB}, PLK1 (polo like kinase 1) [NCBI Gene 5347] {aka PLK, STPK13}
- **Diseases:** Colon Adenocarcinoma (MESH:D003110), cancer (MESH:D009369), cytotoxicity (MESH:D064420), CRC (MESH:D015179)
- **Chemicals:** DPPH (MESH:C004931), Resveratrol (MESH:D000077185), PQM-162 (-), Curcumin (MESH:D003474)
- **Cell lines:** HCT-8 — Homo sapiens (Human), Colon adenocarcinoma, Cancer cell line (CVCL_2478)

## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12649679/full.md

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Source: https://tomesphere.com/paper/PMC12649679