Eupatilin Suppresses Pancreatic Cancer Cells via Glucose Uptake Inhibition, AMPK Activation, and Cell Cycle Arrest

Tae Hyun Park, Hyeon Soo Kim

    Research output: Contribution to journalArticlepeer-review

    10 Citations (Scopus)

    Abstract

    Background/Aim: Pancreatic cancer is one of the most devastating malignancies worldwide. Because of the disappointing outcome of traditional treatment, new drug candidates are being investigated. This study analysed the effect of eupatilin on pancreatic cancer cells. Materials and Methods: Cell viability assay, western blot, siRNA transfection, 2-deoxyglucose uptake assay, AMP/ADP/ATP assay, and fluorescent activated cell sorting were performed. Results: Eupatilin decreased cell viability and activated AMPK in MIA-PaCa2 cells. Eupatilin decreased glucose uptake in pancreatic cancer, which led to cell starvation and AMPK activation. It is well known that AMPK induces p21 and cell cycle arrest by activating p53. In MIA-PaCa2 cells, p53 is mutated and wild-type p53 protein is suppressed. Treatment with eupatilin induced p21 expression but inhibited the expression of mutated p53. Eupatilin activated Tap73, a p53 family member, which can substitute wild-type p53’s role. Conclusion: Eupatilin shows an anticancer effect against pancreatic cancer cells via glucose uptake inhibition, AMPK activation, and cell cycle arrest.

    Original languageEnglish
    Pages (from-to)483-491
    Number of pages9
    JournalAnticancer research
    Volume42
    Issue number1
    DOIs
    Publication statusPublished - 2022 Jan

    Bibliographical note

    Publisher Copyright:
    © 2022 International Institute of Anticancer Research. All rights reserved.

    Keywords

    • AMPK
    • Cell cycle arrest
    • Eupatilin
    • Glucose uptake
    • Tap73

    ASJC Scopus subject areas

    • Oncology
    • Cancer Research

    Fingerprint

    Dive into the research topics of 'Eupatilin Suppresses Pancreatic Cancer Cells via Glucose Uptake Inhibition, AMPK Activation, and Cell Cycle Arrest'. Together they form a unique fingerprint.

    Cite this