Silibinin causes apoptosis and cell cycle arrest in some human pancreatic cancer cells

• Published in: International journal of molecular sciences Vol. 12; no. 8; pp. 4861 - 4871
• Main Authors: Ge, Yakun, Zhang, Yuanxin, Chen, Yunpeng, Li, Quanshun, Chen, Jun, Dong, Ying, Shi, Wei
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.08.2011; Molecular Diversity Preservation International (MDPI)
• Subjects: Antineoplastic Agents - pharmacology; apoptosis; Apoptosis - drug effects; Caspases - metabolism; Cell Cycle Checkpoints - drug effects; Cell Line, Tumor; cell proliferation; Cell Proliferation - drug effects; cell-cycle arrest; Enzyme Activation - drug effects; Humans; Pancreatic cancer; Pancreatic Neoplasms; Pancreatic Neoplasms - metabolism; Silibinin; Silybin; Silymarin - pharmacology; apoptosis; cell-cycle arrest; pancreatic cancer; cell proliferation; Silibinin
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms12084861

Silibinin, an effective anti-cancer and chemopreventive agent in various epithelial cancer models, has been reported to inhibit cancer cell growth through mitogenic signaling pathways. However, whether it can inhibit human pancreatic carcinoma growth and what are the underlying mechanisms is still not well elucidated. Here, we evaluated the inhibitory proliferation effects of Silibinin in pancreatic carcinoma growth and examined whether Silibinin modulates cell cycle and apoptosis. Our results indicate that Silibinin effectively inhibited the pancreatic carcinoma AsPC-1, BxPC-3 and Panc-1 cells' proliferation and caused apoptosis. Silibinin induced a decrease in S phase and cell cycle arrest in G1 phase in AsPC-1 cells, but had no obvious changes in BxPC-3 and Panc-1 cell cycle. Furthermore, these results suggest that Silibinin might be a candidate chemopreventive agent for pancreatic carcinoma therapy.