Comparative study of the cytotoxicity, apoptotic, and epigenetic effects of Boswellic acid derivatives on breast cancer

Fatemeh Jamshidi-adegani, Shokoofeh Ghaemi, Sulaiman Al-Hashmi, Saeid Vakilian, Juhaina Al-kindi, Najeeb Ur Rehman, Khurshid Alam, Khamis Al-Riyami, Rene Csuk, Ehsan Arefian*, Ahmed Al-Harrasi*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

1 Citation (Scopus)

Abstract

This study aimed to compare the effect of Boswellic acid derivatives on the viability, apoptosis, and epigenomic profiling of breast cancer. According to the viability assays, 3-O-acetyl-11-keto-β-Boswellic acid (AKBA) showed more toxicity against MDA-MB-231 cells when compared with the 3-O-acetyl-β-Boswellic acid (ABA). In contrast, ABA revealed less toxicity against MCF-10A. Cell cycle and apoptosis assays determined the maximum apoptotic effect of AKBA on MCF-7, and MDA-MB-231 cells. Interestingly, β-Boswellic acid (BA) and ABA did not promote the apoptosis in MCF-10A cells. Transwell migration assay indicated the greatest normalized inhibition (around 160%) in the migration of MDA-MB-231 cells induced by AKBA. The expression of P53, BAX, and BCL2 genes in cancerous cell lines has affirmed that both AKBA and ABA could induce the maximal apoptosis. Western-blot investigation demonstrated that the maximum over-expression of P53 protein (1.96 times) was caused by AKBA in MDA-MB-231 cells, followed by ABA in MCF-7 cells. The BCL2 protein expression was in agreement with the previously reported results. The global DNA methylation in both cancerous cells was reduced by ABA. These results suggest that ABA represented more epigenetic modulatory effect while AKBA shows more cytotoxic and apoptotic effect against breast cancer cell lines.

Original languageEnglish
Article number19979
Pages (from-to)19979
JournalScientific Reports
Volume12
Issue number1
DOIs
Publication statusPublished - Nov 21 2022

Keywords

  • Epigenomics
  • Tumor Suppressor Protein p53
  • Proto-Oncogene Proteins c-bcl-2
  • Epigenesis, Genetic
  • Neoplasms

ASJC Scopus subject areas

  • General

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