Planta Med 2015; 81 - PW_18
DOI: 10.1055/s-0035-1565642

Exploration of apoptotic effect in cancer cells treated with stingless bee Trigona incisa propolis native to East Kalimantan, Indonesia

PM Kustiawan 1, 2, ET Arung 2, P Phuwapraisirisan 3, S Puthong 4, T Palaga 5, C Chanchao 6
  • 1Program in Biotechnology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand
  • 2Laboratory of Forest Product Technology, Faculty of Forestry, Mulawarman University, Samarinda, Indonesia
  • 3Department of Chemistry, Faculty of Science, Chulalongkorn University, Bangkok, Thailand
  • 4Institute of Biotechnology and Genetic Engineering, Chulalongkorn University, Bangkok, Thailand
  • 5Department of Microbiology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand
  • 6Department of Biology, Faculty of Science, Chulalongkorn University, Bangkok, Thailand

The challenge in the fight against cancer is the non-specific nature of current treatments. The search for specific drugs that are non-cytotoxic to normal cells and can effectively target cancer cells has led some researchers to explore the potential anti-cancer activity of natural compounds. Propolis from honey bee is one of alternative resources that have been traditionally used in indigenous people. However, wild propolis from stingless bee species is not commonly known. This study provides a detailed look at the effect of major compound isolated from Trigona incisa, native stingless bees from Indonesia on cancerous cells. Extraction and partition was by n-hexane, ethyl acetate and methanol, respectively. Then, the cytotoxic activity was checked in lung cancer (Chago), breast cancer (BT-474), liver cancer (Hep-G2), colon cancer (SW620) and gastric (KATO-III) cancer cell lines to lead an active fraction. Then, it was purified by chromatography and analyzed by NMR to identify the compound. We found that the active compound was alkylresorcinol (C21H36O2) or cardol as a major compound from this stingless bee propolis. Our results indicated that cardol induced apoptosis in cancer cells with IC50 of 0.81 ± 0.18 µg/mL (Chago), 4.28 ± 0.14 µg/mL (BT-474), 0.71 ± 0.22 µg/mL (Hep-G2), 4.51 ± 0.76 µg/mL (SW620) and 6.06 ± 0.39 µg/mL (KATO-III). One of the mechanisms by which chemotherapeutics destroy cancer cells is by inducing apoptosis. Here, cardol showed program cell death at early apoptosis (2h, 4h and 6h of incubation) on SW620. Cell arrest in G0/G1 sub phase was observed. This compound specifically in cancer cells may lead to the development of new and more effective cancer fighting agents.