Production of Terretonin N and Butyrolactone I by Thermophilic Aspergillus terreus TM8 Promoted Apoptosis and Cell Death in Human Prostate and Ovarian Cancer Cells

The anticancer activity of terretonin N (1) and butyrolactone I (2), obtained from the thermophilic fungus Aspergillus terreus TM8, was intensively studied against prostate adenocarcinoma (PC-3) and ovary adenocarcinoma (SKOV3) human cell lines. According to this study, both compounds showed potent...

Full description

Saved in:
Bibliographic Details
Published inMolecules (Basel, Switzerland) Vol. 26; no. 9; p. 2816
Main Authors Ghfar, Ayman, El-Metwally, Mohammad, Shaaban, Mohamed, Gabr, Sami, Gabr, Nada, Diab, Marwa, Aqel, Ahmad, Habila, Mohamed, Al-Qahtani, Wahidah, Alfaifi, Mohammad, Elbehairi, Serag, AlJumah, Bayan
Format Journal Article
LanguageEnglish
Published Basel MDPI AG 10.05.2021
MDPI
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The anticancer activity of terretonin N (1) and butyrolactone I (2), obtained from the thermophilic fungus Aspergillus terreus TM8, was intensively studied against prostate adenocarcinoma (PC-3) and ovary adenocarcinoma (SKOV3) human cell lines. According to this study, both compounds showed potent cytotoxicity towards ovarian adenocarcinoma cells (SKOV3) with IC50 1.2 and 0.6 μg/mL, respectively. With respect to metastatic prostate cells (PC-3), the two compounds 1 and 2 showed a significantly promising cytotoxicity effect with IC50 of 7.4 and 4.5 μg/mL, respectively. The tested fungal metabolites showed higher rates of early and late apoptosis with little or no necrotic apoptotic pathway in all treated prostate adenocarcinoma (PC-3) and ovary adenocarcinoma (SKOV3) human cell lines, respectively. The results reported in this study confirmed the promising biological properties of terretonin N (1) and butyrolactone I (2) as anticancer agents via the induction of cellular apoptosis. However, further studies are needed to elucidate the molecular mechanism by which cellular apoptosis is induced in cancer cells.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
ISSN:1420-3049
1420-3049
DOI:10.3390/molecules26092816