Journal
CELLULAR AND MOLECULAR BIOLOGY
Volume 69, Issue 2, Pages 12-18Publisher
C M B ASSOC
DOI: 10.14715/cmb/2023.69.2.3
Keywords
Alpinia japonica; hepatocellular carcinoma; apoptosis; cell cycle checkpoints; activation ofJNK
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Hepatic cancer is the third leading cause of cancer-related death globally, with increasing incidence. Traditional herbal medicine Alpinia japonica (AJ) demonstrated anticancer activity against hepatic cancer cells. AJ extract inhibited cell viability, induced apoptosis, and arrested cell cycle progression in HepG2 cells. Activation of JNK and ERK1/2 pathways played a role in AJ extract-induced cell death and apoptosis. AJ extract has potential as a therapeutic agent for hepatic cancer.
Hepatic cancer was the third most prevalent cause of cancer-related death worldwide in 2018, and its incidence is increasing. While therapeutic agents for hepatic cancer have improved, these agents can cause serious side effects, including damage to healthy tissues. To overcome this limitation, more than 3,000 plants have been used globally as common alternatives for cancer treatment. The anti-cancer activity of Alpinia japonica, one of the traditional herbal medicines (Korean name: Kkot-yang-ha), was investigated. Water extract of A. japonica (AJ) decreased the cell viability of hepatic cancer cells. AJ extract showed greater than 70% loss of mitochondrial potential in HepG2 cells as demonstrated by JC-1 staining. Apoptosis was induced by treatment with AJ extract as shown through FACS analysis, and G0/G1 phase arrest of 76.66% HepG2 cells was confirmed through cell cycle analysis and quantitative RT-PCR. Improper regulation of ERK1/2 might contribute to cell death, and JNK activation is necessary for apoptosis induced by stress stimuli. AJ extract stimulated the phosphorylation of JNK and ERK1/2, mitogen-activated protein kinases (MAPKs), in HepG2 cells. AJ extract has anticancer activity by inhibiting cell cycle progression, leading to apoptosis of hepatic cancer cells. This extract could potentially be used as a therapeutic agent for hepatic cancer.
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