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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. [ABSTRACT FROM AUTHOR]

Saikosaponin D (SSD), derived from Bupleurum falcatum L., has various pharmacological properties, including immunoregulatory, anti-inflammatory, and anti-allergic effects. Several studies have investigated the anti-tumor effects of SSD on cancer in multiple organs. However, its role in colorectal cancer (CRC) remains unclear. Therefore, this study aimed to elucidate the suppressive effects of SSD on CRC cell survival and metastasis. SSD reduced the survival and colony formation ability of CRC cells. SSD-induced autophagy and apoptosis in CRC cells were measured using flow cytometry. SSD treatment increased LC3B and p62 autophagic factor levels in CRC cells. Moreover, SSD-induced apoptosis occurred through the cleavage of caspase-9, caspase-3, and PARP, along with the downregulation of the Bcl-2 family. In the in vivo experiment, a reduction in the number of metastatic tumor nodules in the lungs was observed after the oral administration of SSD. Based on these results, SSD inhibits the metastasis of CRC cells to the lungs by inducing autophagy and apoptosis. In conclusion, SSD suppressed the proliferation and metastasis of CRC cells, suggesting its potential as a novel substance for the metastatic CRC treatment. [ABSTRACT FROM AUTHOR]