Abstract Title:

Cucurbitacin D inhibits the proliferation of HepG2 cells and induces apoptosis by modulating JAK/STAT3, PI3K/Akt/mTOR and MAPK signaling pathways.

Abstract Source:

Curr Cancer Drug Targets. 2022 Jun 23. Epub 2022 Jun 23. PMID: 35786188

Abstract Author(s):

Muhammed MehdiÜremiş, Nuray Üremiş, Emir Tosun, Merve Durhan, Yılmaz Çiğremiş, Ahmet Baysar, Yusuf Türköz

Article Affiliation:

Muhammed MehdiÜremiş


BACKGROUND: Cucurbitacin D (CuD) is a natural compound that can be isolated in various plant families, mainly from Ecballium Elaterium (L.) A. Rich. (E. Elaterium). It is a triterpenoid with a broad spectrum of biological activity, including anti-cancer properties. Hepatocellular carcinoma, the aggressive type of liver cancer, is an important public health problem worldwide.

OBJECTIVE: In the present study, we investigated the anticancer effect of CuD treated at different doses on the HepG2 cell line and the underlying mechanism in vitro.

METHOD: CuD was isolated from the fruit juice of E. Elaterium plant and quantitative analysis was performed using high-performance liquid chromatography. The cell viability effect of purified CuD was determined by the MTT test also cell apoptosis and cell cycle arrest effects were determined by flow cytometry. DNA damage was evaluated with the comet test. Proteins and genes involved in PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 signaling pathways were evaluated by western blot and qRT-PCR.

RESULT: CuD showed both antiproliferative and cytotoxic effects against the HepG2 cell line in a dose and time-dependent manner. It was observed that CuD induced apoptosis and blocked the cell cycle in HepG2 cells. It was observed that the expression of genes and some proteins that play a key role in PI3K/AKT/mTOR, MAPK, and JAK2/STAT3 cascades were dose-dependently down-regulated and activated the apoptotic pathway.

CONCLUSION: All these results; show promise that CuD may have a therapeutic effect in liver cancer with HCC.

Study Type : In Vitro Study

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