Arcyriaflavin A Decreases Endometriosis Cell Viability and Proliferation

Arcyriaflavin A shows promise as a potential therapy to treat Endometriosis.

Key Points

Highlights:

• Laboratory tests have shown that the introduction of Arcyriaflavin A to Endometriosis stromal cells led to a statistically significant decrease in Endometriosis cell viability and proliferation.
• Arcyriaflavin A also increased apoptosis rates and reduced proliferation rates.

What’s done here?

• Endometriotic cyst stromal cells were isolated from 32 patients. The cells from each patient were separated into four different groups. One control group that received no treatment and three Arcyriaflavin A treatment groups which received .1, 1, or 10 µM of Arcyriaflavin A respectively.
• Cell viability, proliferation, apoptosis rates, and cell cycle arrest were determined for each treatment group and compared to the control group to determine any statistically significant differences.

Key results:

• When compared to the control group, Arcyriaflavin A significantly reduced endometriosis stromal cell proliferation in doses as small as 1 µM and significantly increased apoptosis rates in the 10 µM treatment group.
• When compared to the control group, the 10 µM treatment group displayed a higher percentage of cells stuck in the G0 and G1 phases of the cell cycle and significantly fewer cells in the S or M phases of the cycle. These results imply that cell cycle arrest rates increase and cell division decreases due to Arcyriaflavin A.

Importance:

• Endometriosis cells exhibit proliferative, antiapoptotic, angiogenic, and fibrogenic features.
• Cyclin D1 and cyclin-dependent kinase (CDK), regulate cell cycle progression from the G1 phase to the S phase. Authors hypothesized that cyclin D1 and CDK inhibitors might alleviate endometriosis, and used Arcyriaflavin A, a representative cyclin D1–CDK4 inhibitor, to examine its inhibition effect on cyclin D1–CDK4 in endometriosis.
• The results indicate that Arcyriaflavin A may be a potential therapy for patients who suffer from Endometriosis.

Limitations:

• Further testing is needed to ensure the in-vitro benefits of Arcyriaflavin A treatment can be safely replicated in-vivo.
• The exact method by which the Endometriosis cells were treated with Arcyriaflavin A was not properly described, so we do not know the precise method that led to these promising results.
• The effects of Arcyriaflavin A were only tested on Endometriotic cyst stromal cells. Further testing must be done in order to ensure Arcyriaflavin A’s therapeutic effects can treat all types of cells of endometriosis.

Lay Summary

The purpose of this research topic was to determine whether Arcyriaflavin A could serve as a potential new therapeutic option for those suffering from Endometriosis. Arcyriaflavin A is a Cyclin D1 inhibitor. Cyclin D1 regulates the cell cycle by interacting with the enzymes CDK4 and CDK6. Therefore, a Cyclin D1 inhibitor, like Arcyriaflavin A has the potential to disrupt the cell cycle by indirectly affecting the enzymes that regulate the cycle.

In this experiment, Endometriotic cyst stromal cells were collected from 32 patients. The cells from each patient were then broken into four test groups which included an untreated control group and 3 treatment groups that received .1, 1, and 10 µM of Arcyriaflavin A treatment respectively The research team then used various scientific assays to determine any differences in cell viability, proliferation, apoptosis rates, and cell cycle arrest rates in the Arcyriaflavin A treated groups compared to the control group.

The results indicate that Arcyriaflavin A treatment led to increased apoptosis rates and decreased cell viability. The treatment also led to high rates of cell cycle arrest and lower levels of cell division and proliferation.

These promising results indicate that Arcyriaflavin A can potentially be an effective treatment against Endometriosis. However, further testing must be done in order to ensure the in-vitro results of this experiment can be safely replicated in-vivo.

Research Source: https://www.ncbi.nlm.nih.gov/pubmed/28720098