Abstract
Gastric cancer most commonly occurs in East Asia, and China accounts for more than half the of world's gastric cancer burden. Despite the efficacy of chemotherapy for patients, this treatment leads to significant patient inconvenience, toxicity and cost. The present study aimed to assess a non-toxic agent, glabridin, as a future chemotherapeutic approach for treating gastric cancer. Using cell proliferation, apoptosis, invasion, and colony formation assays, it was determined that glabridin alone, or in combination with 5-fluorouracil (5-FU), inhibited MKN-45 cell proliferation and invasion, and increased apoptosis. These effects were accompanied by downregulation of p16, E-cadherin and apoptosis regulator Bcl-2 protein, and upregulation of N-cadherin, apoptosis regulator BAX and caspases 3, 8 and 9. The results demonstrated that glabridin may inhibit the malignant proliferation of the human gastric cancer MKN-45 cell line and enhance the efficiency of 5-FU. The data indicate that the p16, and potentially the p16/cyclin-dependent kinase 4/cyclin D1 pathway, may be a novel target for gastric cancer therapy.