2. Academic Validation
  3. Anticancer activity of synthetic (±)-kusunokinin and its derivative (±)-bursehernin on human cancer cell lines

Anticancer activity of synthetic (±)-kusunokinin and its derivative (±)-bursehernin on human cancer cell lines

  • Biomed Pharmacother. 2019 Sep;117:109115. doi: 10.1016/j.biopha.2019.109115.
Thidarath Rattanaburee 1,  Tienthong Thongpanchang 2,  Krittaphat Wongma 3,  Aman Tedasen 1,  Yaowapa Sukpondma 4,  Potchanapond Graidist 5
Affiliations

Affiliations

  • 1 Department of Biomedical Sciences, Faculty of Medicine, Prince of Songkla University, Songkhla, 90110, Thailand.
  • 2 Department of Chemistry, Faculty of Science and Center of Excellence for Innovation in Chemistry, Mahidol University, Bangkok, 10400, Thailand.
  • 3 General Sciences Program, Faculty of Education, Sakon Nakhon Rajabhat University, Sakon Nakhon, 47000, Thailand.
  • 4 Department of Chemistry and Center of Excellence for Innovation in Chemistry, Faculty of Science, Prince of Songkla University, Songkhla 90110, Thailand.
  • 5 Department of Biomedical Sciences, Faculty of Medicine, Prince of Songkla University, Songkhla, 90110, Thailand; The Excellent Research Laboratory of Cancer Molecular Biology, Prince of Songkla University, Songkhla, 90110, Thailand. Electronic address: [email protected].
PMID: 31220743 DOI: 10.1016/j.biopha.2019.109115
Abstract

Kusunokinin is a potent lignan compound with a several biological properties including antitrypanosomal and Anticancer. In this study, (±)-kusunokinin and its derivative, (±)-bursehernin, were synthesized and investigated for their Anticancer activities on cell viability, cell cycle arrest and Apoptosis in Cancer cell lines including breast Cancer (MCF-7, MDA-MB-468 and MDA-MB-231), colon Cancer (HT-29) and cholangiocarcinoma (KKU-K100, KKU-M213 and KKU-M055) cells. The result showed that (±)-kusunokinin and (±)-bursehernin represented the strongest growth inhibition against breast Cancer (MCF-7) and cholangiocarcinoma (KKU-M213) cells with the IC50 values of 4.30 ± 0.65 μM and 3.70 ± 0.79 μM, respectively, both of which were lower than IC50 of normal fibroblast cells (L929). Etoposide was used as a positive control since this chemotherapeutic drug is in the lignan group same as (±)-kusunokinin. Surprisingly, etoposide showed less cytotoxicity than (±)-kusunokinin and its derivative on MCF-7, HT-29, KKU-M213 and KKU-K100. Moreover, (±)-bursehernin induced cell cycle arrest at G2/M phase, meanwhile (±)-kusunokinin tended to increased cell population at G2/M phase but did not show the significant difference compared with non-treated cells. Interestingly, protein levels related to cell proliferation pathway (Topoisomerase II, STAT3, cyclin D1, and p21) were significantly decreased at 72 h. Both compounds induced apoptotic cell in time-dependent manner as confirmed by MultiCaspase assay. In conclusion, synthetic compound, (±)-kusunokinin and (±)-bursehernin, showed Anticancer effects via the reduction of cell proliferation proteins and induction of Apoptosis.

Keywords

Anticancer; Bursehernin; Kusunokin.

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