The Inhibitory Effect of Kerra[sup.TM], KS[sup.TM], and Minoza[sup.TM] on Human Papillomavirus Infection and Cervical Cancer

• Published in: Medicina (Kaunas, Lithuania) Lithuania), 2023-12, Vol.59 (12)
• Main Authors: Choowongkomon, Kiattawee, Choengpanya, Khuanjarat, Pientong, Chamsai, Ekalaksananan, Tipaya, Talawat, Sulak, Srathong, Pussadee, Chuerduangphui, Jureeporn
• Format: Article
• Language: English
• Subjects: Cervical cancer; Development and progression; Health aspects; Infection; Papillomavirus infections; Papillomaviruses; Prevention; Resveratrol
• ISSN: 1648-9144
• DOI: 10.3390/medicina59122169

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, Kerra[sup.TM], KS[sup.TM], and Minoza[sup.TM], were studied on HeLa and CaSki cells. Materials and Methods: The effects of Kerra[sup.TM], KS[sup.TM], and Minoza[sup.TM] 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 Kerra[sup.TM] being the most potent anticancer agent followed by KS[sup.TM] and Minoza[sup.TM]. Kerra[sup.TM] 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 KS[sup.TM] at 261 µg/mL efficiently inhibited viral infection in both pre-attachment and adsorption steps. However, Kerra[sup.TM], KS[sup.TM], and Minoza[sup.TM] 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 Kerra[sup.TM] increased population of dead cells in dose-dependent manner in both CaSki and HeLa. The percentage of secondary necrosis in Kerra[sup.TM]-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 Kerra[sup.TM] than CaSki. For KS[sup.TM] and Minoza[sup.TM], these extracts at 250 µg/mL promoted autophagy over cell death. At 500 µg/mL, the percentage of dead cells in Kerra[sup.TM] was higher than that of KS[sup.TM] and Minoza[sup.TM]. Conclusions: Kerra[sup.TM] is a potent traditional medicine for promoting cancer cell death. Kerra[sup.TM] 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.