Sesamin induces cell cycle arrest and apoptosis through the inhibition of signal transducer and activator of transcription 3 signalling in human hepatocellular carcinoma cell line HepG2

Biol Pharm Bull. 2013;36(10):1540-8. doi: 10.1248/bpb.b13-00235.


Sesamin, one of the most abundant lignans in sesame seeds, has been shown to exhibit various pharmacological effects. The aim of this study was to elucidate whether sesamin promotes cell cycle arrest and induces apoptosis in HepG2 cells and further to explore the underlying molecular mechanisms. Here, we found that sesamin inhibited HepG2 cell growth by inducing G2/M phase arrest and apoptosis. Furthermore, sesamin suppressed the constitutive and interleukin (IL)-6-induced signal transducer and activator of transcription 3 (STAT3) signalling pathway in HepG2 cells, leading to regulate the downstream genes, including p53, p21, cyclin proteins and the Bcl-2 protein family. Our studies showed that STAT3 signalling played a key role in sesamin-induced G2/M phase arrest and apoptosis in HepG2 cells. These findings provided a molecular basis for understanding of the effects of sesamin in hepatocellular carcinoma tumour cell proliferation. Therefore, sesamin may thus be a potential chemotherapy drug for liver cancer.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antineoplastic Agents, Phytogenic / pharmacology
  • Antineoplastic Agents, Phytogenic / therapeutic use
  • Apoptosis / drug effects*
  • Carcinoma, Hepatocellular / drug therapy
  • Carcinoma, Hepatocellular / genetics
  • Carcinoma, Hepatocellular / metabolism*
  • Cell Cycle / drug effects
  • Cell Cycle Checkpoints / drug effects*
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • Cyclins / genetics
  • Cyclins / metabolism
  • Dioxoles / pharmacology*
  • Dioxoles / therapeutic use
  • Gene Expression Regulation, Neoplastic / drug effects
  • Hep G2 Cells
  • Humans
  • Interleukin-6 / metabolism
  • Lignans / pharmacology*
  • Lignans / therapeutic use
  • Liver Neoplasms / drug therapy
  • Liver Neoplasms / genetics
  • Liver Neoplasms / metabolism*
  • Phytotherapy
  • Plant Extracts / pharmacology
  • Plant Extracts / therapeutic use
  • STAT3 Transcription Factor / antagonists & inhibitors*
  • Seeds
  • Sesamum / chemistry*
  • Signal Transduction
  • Tumor Suppressor Protein p53 / metabolism


  • Antineoplastic Agents, Phytogenic
  • Cyclin-Dependent Kinase Inhibitor p21
  • Cyclins
  • Dioxoles
  • Interleukin-6
  • Lignans
  • Plant Extracts
  • STAT3 Transcription Factor
  • Tumor Suppressor Protein p53
  • sesamin