Related Experiment Video
Updated: Apr 15, 2026

Use of Interferon-γ Enzyme-linked Immunospot Assay to Characterize Novel T-cell Epitopes of Human Papillomavirus
Published on: March 8, 2012
Activity of Andrographolide and Its Derivatives on HPV16 Pseudovirus Infection and Viral Oncogene Expression in
Tipaya Ekalaksananan1, Waree Sookmai, Supada Fangkham
1a Department of Microbiology, Faculty of Medicine, HPV & EBV and Carcinogenesis Research Group, Khon Kaen University , Khon Kaen , Thailand.
Abstract:
Andrographolide (Androg) has been reported to contain antiviral and antitumor activities, but the effects of Androg on human papillomavirus (HPV) infection and cervical cancer have not been elucidated. This study investigated the effects of Androg and its derivatives, namely, 14-deoxy-11,12-didehydroandrographolide (14-DDA) and 3,19-isopropylidene andrographolide (IPAD), on HPV16 pseudovirus (HPV16PsV) infectivity, HPV16 E6 oncogene expression and cervical cancer cell apoptosis. The result demonstrated that all compounds inhibited HPV16PsV infection and that 14-DDA showed the highest potency. Only Androg suppressed long control region (LCR) transcription activity of HPV16 in transiently transfected C33A cells and significantly inhibited E6 oncogene expression in SiHa cells in a dose-dependent manner. A twofold subcytotoxic concentration of IPAD exhibited an inhibitory effect on E6 oncogene expression at 48-h posttreatment. Interestingly, p53 protein was restored in a downstream process and was detected earlier by IPAD treatment than by Androg treatment. This result corresponded to the level of cell apoptosis and cell cycle arrest at the G2/M phase. E6 oncogene expression was also suppressed in CaSki cells treated with Androg and IPAD leading to cell apoptosis. These findings imply that Androg and its derivatives have different activities and may be effective agents for HPV prevention and cervical cancer treatment.
Insights
Andrographolide and its derivatives inhibit human papillomavirus (HPV) infection and cervical cancer progression by suppressing viral oncogene expression and promoting apoptosis.
Area of Science:
- Phytochemistry
- Virology
- Oncology
Background:
- Andrographolide (Androg) exhibits antiviral and antitumor properties.
- The impact of Androg and its derivatives on human papillomavirus (HPV) infection and cervical cancer remains unclear.
Purpose of the Study:
- To investigate the effects of Androg, 14-deoxy-11,12-didehydroandrographolide (14-DDA), and 3,19-isopropylidene andrographolide (IPAD) on HPV16 pseudovirus (HPV16PsV) infectivity.
- To assess the impact of these compounds on HPV16 E6 oncogene expression and cervical cancer cell apoptosis.
Main Methods:
- Treatment of C33A, SiHa, and CaSki cells with Androg, 14-DDA, and IPAD.
- Assay of HPV16PsV infectivity.
- Measurement of HPV16 long control region (LCR) transcription activity.
- Quantification of E6 oncogene expression and p53 protein levels.
- Analysis of cell apoptosis and cell cycle arrest.
Main Results:
- All tested compounds inhibited HPV16PsV infection, with 14-DDA showing the highest potency.
- Androg suppressed HPV16 LCR transcription and E6 oncogene expression in a dose-dependent manner.
- IPAD and Androg treatments restored p53 protein levels, induced cell apoptosis, and caused G2/M phase cell cycle arrest.
Conclusions:
- Androg and its derivatives demonstrate distinct activities against HPV infection and cervical cancer.
- These compounds show potential as therapeutic agents for HPV-related diseases and cervical cancer treatment.
More Related Videos
Related Concept Videos
Cancer Vaccines
Cancer vaccines come in two categories: preventive (prophylactic) and treatment (active). Preventive vaccines, such as the Human Papillomavirus (HPV) vaccine, protect against viruses that cause certain...
Inhibition of Cdk Activity
Inhibitors of Viral Protein Synthesis
Rous Sarcoma Virus (RSV) and Cancer
RSV is a retrovirus that contains two copies of a plus-strand RNA genome. Its genome consists of four main open...
Mechanisms of Retrovirus-induced Cancers
Mechanisms of Retrovirus-induced Cancers

