Increased Oxidative Stress in Endometriosis may Be Linked to Higher Risk of Ovarian Cancer

Increased Oxidative Stress in Endometriosis may Be Linked to Higher Risk of Ovarian Cancer

Increased oxidative stress might contribute to higher risk of ovarian cancer in women with endometriosis, a new study found.

In the study that was published in the scientific journal Translational Oncogenomics, a group of researchers led by Dr. Hariyono Winarto from the Universitas Indonesia in Jakarta identified increased oxidative stress as one of the causes that might explain the higher incidence of endometriosis-associated ovarian cancers.

The normal process of respiration in our cells creates reactive oxygen species (ROS) in every organ and tissue. ROS are very reactive molecules that can damage the components of our cells such as lipids (fat compounds that form the cell membranes), proteins and the DNA. When parts of the DNA that make up genes that are important to suppress the formation of tumors is damaged, cancer can occur. AT-rich interactive domain 1A (ARID1A) is one such tumor-suppressor gene that is often mutated in endometriosis-associated ovarian cancer.

To counteract ROS, our body naturally produces antioxidant proteins. However, when in certain organs or tissues a number of antioxidants produced are not enough to overcome the effects of ROS, oxidative stress and cellular damage occur.

One of these antioxidant proteins is manganese superoxide dismutase (MnSOD). If there is not enough MnSOD protein in the body, the chemical compound malondialdehyde (MDA) derived from the oxidation of lipids accumulates in tissues. Measuring the amount of MDA can, therefore, help researchers measure oxidative damage.

The authors of the study investigated the expression of the ARID1A gene in comparison to the amounts of MnSOD and of MDA in human samples. They measured normal endometrial tissues, tissues from patients with endometriosis, tissues from patients with endometriosis-associated ovarian cancer, and tissues from patients with non-endometriosis-associated ovarian cancer.  

In addition, they tested how the expression of the AID1A gene changed in response to oxidative stress in cells cultured from patients with endometriosis and in cultures of normal endometrial cells.

They found that the expression of the ARID1A gene in patients with non-endometriosis-associated ovarian cancer was extremely variable. However, the expression of ARID1A was always lower in samples from patients with endometriosis and those with endometriosis-associated ovarian cancer, than in normal endometrial tissue.

The authors also proved that by increasing oxidative stress they could reduce ARID1A expression in cells derived from an individual with endometriosis but also from cultures of normal endometrial cells.

These results suggest that the low expression levels of the ARID1A gene in endometriotic tissue may be one of the causes responsible for the higher incidence of cancer in women with endometriosis.


Research Source:

Increased Oxidative Stress Ovarian Cancer


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