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Adv Pharm Bull. 2020;10(4): 638-647.
doi: 10.34172/apb.2020.077
PMID: 33062604
PMCID: PMC7539315
Scopus ID: 85090451182
  Abstract View: 1176
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Research Article

Transcriptome Changes in Colorectal Cancer Cells upon Treatment with Avicequinone B

Yanet Ocampo 1 ORCID logo, Daneiva Caro 1 ORCID logo, David Rivera 1, Jhoan Piermattey 2, Ricardo Gaitán 2, Luis A. Franco 1* ORCID logo

1 Biological Evaluation of Promising Substances Group, Department of Pharmaceutical Sciences, University of Cartagena, Carrera 50 No. 29-11, 130014, Cartagena, Colombia.
2 Natural Products Group, Department of Pharmaceutical Sciences, University of Cartagena, Carrera 50 No. 29-11, 130014, Cartagena, Colombia.
*Corresponding Author: *Corresponding Author: Luis A. Franco, Tel: 57-5-6699771, Fax: 57-5-6698323, Email: , Email: lfrancoo@unicartagena.edu.co

Abstract

Purpose: Naphtho[2,3-b]furan-4,9-dione (Avicequinone B), a natural naphthoquinone isolated from the mangrove tree Avicennia alba, is recognized as a valuable synthetic precursor with anti-proliferative effect. However, the molecular mechanism involved in its bioactivity has not been investigated. This study aimed to determine the selectivity of avicequinone B against cancer cells and the transcriptomic changes induced in colorectal cancer (CRC).

Methods: The cytotoxic effect against adenocarcinoma-derived cells or fibroblasts was evaluated using MTT assay. In addition, CRC cells were treated with avicequinone B in different settings to evaluate colony-forming ability, cell cycle progression, apoptosis/necrosis induction, and transcriptome response by RNA-seq.

Results: Avicequinone B effectively reduced the viability of breast, colorectal, and lung adenocarcinoma cells with IC50 lower than 10 μM, while fibroblasts were less affected. The induction of G2/M arrest and necrosis-like cell death were observed in avicequinone B-treated HT-29 cells. Furthermore, RNA-seq revealed 490 differentially expressed genes, highlighting the reduction of interferon stimulated genes and proliferative signaling pathways (JAK-STAT, MAPK, and PI3K-AKT), as well as the induction of ferroptosis and miR-21 expression.

Conclusion: In short, these results demonstrated the therapeutic potential of avicequinone B and paved the foundation for elucidating its mechanisms in the context of CRC.

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Submitted: 22 Oct 2019
Revision: 04 Jan 2020
Accepted: 27 Jan 2020
ePublished: 09 Aug 2020
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