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Antiausterity Activity of Secondary Metabolites from the Roots of Ferula hezarlalehzarica against the PANC-1 Human Pancreatic Cancer Cell Line

Authors
  • Alilou, Mostafa1, 2
  • Dibwe, Dya Fita3
  • Schwaiger, Stefan1
  • Khodami, Mojtaba4
  • Troppmair, Jakob2
  • Awale, Suresh3
  • Stuppner, Hermann1
  • 1 University of Innsbruck, Austria , (Austria)
  • 2 Innsbruck Medical University, Austria , (Austria)
  • 3 University of Toyama, Japan , (Japan)
  • 4 Kerman University of Medical Science, Iran
Type
Published Article
Journal
Journal of Natural Products
Publisher
American Chemical Society
Publication Date
Mar 12, 2020
Volume
83
Issue
4
Pages
1099–1106
Identifiers
DOI: 10.1021/acs.jnatprod.9b01109
PMID: 32163286
PMCID: PMC7307951
Source
PubMed Central
License
Unknown

Abstract

Human pancreatic cancer is one of the most aggressive types of cancer, with a high mortality rate. Due to the high tolerance of such cancer cells to nutrient starvation conditions, they can survive in a hypovascular tumor microenvironment. In this study, the dichloromethane extract of the roots of Ferula hezarlalehzarica showed potent preferential cytotoxic activity with a PC50 value of 0.78 μg/mL. Phytochemical investigation of this extract led to the isolation of 18 compounds, including one new sesquiterpenoid ( 6 ) and one new monoterpenoid ( 18 ). All isolated compounds were evaluated for their preferential cytotoxicity against PANC-1 human pancreatic cancer cells by employing an antiausterity strategy. Among them, ferutinin ( 2 ) was identified as the most active compound, with a PC50 value of 0.72 μM. In addition, the real-time effect of ferutinin ( 2 ) and compound 6 against PANC-1 cells, exposed to a nutrient-deprived medium (NDM), showed cell shrinkage, leading to cancer cell death within a short period of exposure. Compounds 2 and 6 also inhibited colony formation of PANC-1 cells. The present study indicates that the dichloromethane extract of the roots of F. hezarlalehzarica is a rich source of bioactive compounds for targeting PANC-1 cells.

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