Kiattawee Choowongkomon

Chamuangone from Garcinia cowa leaves inhibits cell proliferation and migration and induces cell apoptosis in human cervical cancer in vitro

Abstract Objectives To examine the effects of chamuangone on human cancer cell proliferation, migration and apoptosis. Methods An MTT assay was used to study the effect of chamuangone on human cervical carcinoma cell growth. An in-vitro scratch migration assay was used to investigate the activity of cell motility after chamuangone treatment. Chamuangone-induced cell apoptosis in HeLa cells was determined using the apoptotic assay kit. The inhibitory activities of chamuangone were examined by ADP-Glo™ kinase assay. The GOLD docking algorithm was used to demonstrate the mechanism against tyrosine kinase of EGFR. Key findings Chamuangone showed a strong inhibitory cell proliferation of HeLa cells with IC50 values of 3.59 µm and effectively inhibited HeLa cell migration. In addition, chamuangone exhibited the apoptotic cell death induction in a time and dose-dependent manner. Finally, chamuangone also was tested for EGFR-TK inhibition activity. The IC50 value of chamuangone was 2.85 nm, whereas the IC50 value of gefitinib was 15.10 nm. Conclusions The above results confirm the inhibitory effects of chamuangone on HeLa cell proliferation and cell migration. In addition, chamuangone also induces cell apoptosis in HeLa cells. These findings indicate that chamuangone is a compound that is a potential chemotherapeutic agent.

The Inhibitory Effect of KerraTM, KSTM, and MinozaTM on Human Papillomavirus Infection and Cervical Cancer

Background and Objectives: Cervical cancer is one of the most common types of frequently found cancers in Thailand. One of the causative agents is the infection of the high-risk human papillomavirus (HPV) type 16 and 18. Traditional medicines are rich sources of bioactive compounds which are a valuable source for the development of novel cancer therapies. In this study, the therapeutic effects of 3 traditional medicines, KerraTM, KSTM, and MinozaTM, were studied on HeLa and CaSki cells. Materials and Methods: The effects of KerraTM, KSTM, and MinozaTM on cancer cells were evaluated through cytotoxicity and cell death assays. The infection assay using HPV-16 pseudovirus was also carried out. Results: All traditional medicines efficiently suppressed cell growths of HeLa and CaSki, with KerraTM being the most potent anticancer agent followed by KSTM and MinozaTM. KerraTM at 158 µg/mL and 261 µg/mL significantly increases the percentage inhibition of the HPV-16 pseudovirus infection in a pre-attachment step in a dose-dependent manner, while KSTM at 261 µg/mL efficiently inhibited viral infection in both pre-attachment and adsorption steps. However, KerraTM, KSTM, and MinozaTM at subtoxic concentrations could not reduce the viral E6 mRNA expressions of HPV-16 and HPV-18. Cell death assay by acridine orange/ethidium bromide showed that KerraTM increased population of dead cells in dose-dependent manner in both CaSki and HeLa. The percentage of secondary necrosis in KerraTM-treated CaSki was higher than that of HeLa cells, while the percentage of late apoptotic cells in HeLa was higher than that of CaSki, indicating that HeLa was more susceptible to KerraTM than CaSki. For KSTM and MinozaTM, these extracts at 250 µg/mL promoted autophagy over cell death. At 500 µg/mL, the percentage of dead cells in KerraTM was higher than that of KSTM and MinozaTM. Conclusions: KerraTM is a potent traditional medicine for promoting cancer cell death. KerraTM is possibly useful in the prevention and treatment of cervical cancer. Further investigation will be carried out to gain a better understanding of the biochemical mechanism and the pharmacological activity underlying this effect.