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Apoptosis and Metabolic Reprogramming by RHART in Hepatocellular Carcinoma Through the CPSF6/MCT4/c-Myc Signaling

Youngsang Park¹, Su-Yeon Park¹, Bonglee Kim¹

¹College of Korean Medicine, Kyung Hee University, Seoul, Republic of Korea.

Phytotherapy Research : PTR

|February 18, 2026

Summary

Rhus verniciflua and Artemisia capillaris extract (RHART) induces liver cancer cell death by targeting key proteins like CPSF6, MCT4, and c-Myc. This natural compound shows potential for treating hepatocellular carcinoma.

Area of Science:

Biochemistry
Molecular Biology
Oncology

Background:

Hepatocellular carcinoma (HCC) remains a significant health challenge with limited therapeutic options.
Traditional herbal medicines like Rhus verniciflua and Artemisia capillaris have been used for liver ailments, but their molecular mechanisms are not well understood.
The ethanol extract of Rhus verniciflua and Artemisia capillaris (RHART) is investigated for its anti-cancer effects in HCC.

Purpose of the Study:

To elucidate the apoptotic and metabolic reprogramming mechanisms of RHART in hepatocellular carcinoma.
To investigate RHART's regulation of oncogenic drivers: cleavage and polyadenylation specificity factor 6 (CPSF6), monocarboxylate transporter 4 (MCT4), and c-Myc.
To explore the impact of RHART on glycolysis-related pathways in HCC.

Main Methods:

Standardization of RHART using High-Performance Liquid Chromatography (HPLC) fingerprinting.
In vitro analysis of cytotoxicity, apoptosis, and protein expression in HCC cell lines (Hep3B, Huh7) using MTT, cell cycle, and Western blot assays.
In vivo validation using Hep3B xenografts in nude mice, followed by immunohistochemistry and functional rescue assays.

Main Results:

RHART treatment induced significant cytotoxicity and apoptosis in HCC cells, evidenced by increased sub-G1 population and cleaved caspase-3.
RHART downregulated key proteins including CPSF6, MCT4, c-Myc, and glycolytic enzymes (HK2, PKM2, LDHA), reducing glucose uptake and lactate production.
RHART suppressed tumor growth in vivo and modulated the expression of proliferation and apoptosis markers.

Conclusions:

RHART exerts anti-cancer effects in hepatocellular carcinoma by inducing apoptosis and metabolic reprogramming.
The mechanism involves targeting the CPSF6/MCT4/c-Myc signaling axis.
RHART demonstrates potential as a novel natural therapeutic agent for liver cancer.

Keywords:

CPSF6 MCT4 RHART extract glycolysis hepatocellular carcinoma

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