Nutrients · 2024
Inhibitory Effect of Alnustone on Survival and Lung Metastasis of Colorectal Cancer Cells.
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Park Shin-Young, Mun Jeong-Geon, Lee Yoon-Seung, Lee Sun-Bin, Kim Su-Jin, Jang Jeong-Ho, Kim Ho-Yoon, Hong Seung-Heon, Kee Ji-Ye
Аннотация
BACKGROUND/OBJECTIVES: Alnustone (Aln) is an effective compound of Alpinia katsumadae Hayata. Aln possesses various pharmacological activities such as antibacterial, anti-inflammatory, and anti-cancer effects. However, the inhibitory effect of Aln on colorectal cancer (CRC) has not yet been identified. Thus, research was conducted to clarify whether Aln can suppress the proliferative and metastatic ability of CRC cells.
METHODS: A cell viability assay was performed to confirm the decrease in CRC cell viability following Aln treatment. Flow cytometry was carried out to evaluate the effects of Aln on cell cycle arrest, autophagy, and apoptosis in CRC cells. In addition, a lung metastasis animal model was used to check the inhibitory effect of Aln on the metastasis of CRC cells.
RESULTS: Aln remarkably diminished the viability and colony-forming ability of several CRC cell lines. In addition, Aln led to a halt at the G0/G1 phase through downregulating cyclin D1-CDK4 in CRC cells. The upregulation of LC3B and p62 expression by Aln triggered autophagy of CRC cells. Moreover, Aln promoted mitochondrial depolarization, resulting in apoptosis of CRC cells. Oral administration of Aln significantly restrained the metastasized lung tumor nodules.
CONCLUSIONS: This study demonstrated that Aln can suppress the survival and lung metastasis of CRC cells by promoting cell cycle arrest, autophagy, and apoptosis.
METHODS: A cell viability assay was performed to confirm the decrease in CRC cell viability following Aln treatment. Flow cytometry was carried out to evaluate the effects of Aln on cell cycle arrest, autophagy, and apoptosis in CRC cells. In addition, a lung metastasis animal model was used to check the inhibitory effect of Aln on the metastasis of CRC cells.
RESULTS: Aln remarkably diminished the viability and colony-forming ability of several CRC cell lines. In addition, Aln led to a halt at the G0/G1 phase through downregulating cyclin D1-CDK4 in CRC cells. The upregulation of LC3B and p62 expression by Aln triggered autophagy of CRC cells. Moreover, Aln promoted mitochondrial depolarization, resulting in apoptosis of CRC cells. Oral administration of Aln significantly restrained the metastasized lung tumor nodules.
CONCLUSIONS: This study demonstrated that Aln can suppress the survival and lung metastasis of CRC cells by promoting cell cycle arrest, autophagy, and apoptosis.
Предметные рубрики MeSH
Colorectal NeoplasmsHumansLung NeoplasmsAnimalsAutophagyApoptosisCell SurvivalCell Line, TumorMiceCell ProliferationCyclin-Dependent Kinase 4Cyclin D1Cell Cycle CheckpointsMice, Inbred BALB CXenograft Model Antitumor AssaysMice, NudeAlpiniaMaleMembrane Potential, MitochondrialMicrotubule-Associated Proteins