UT Arlington biochemists say their newly published study brings researchers a step closer to understanding how the commonly used synthetic compound bisphenol-A, or BPA, may promote breast cancer growth.
Subhrangsu Mandal, associate professor of chemistry/biochemistry, and Arunoday Bhan, a Ph.D. student in Mandal’s lab, looked at a molecule called RNA HOTAIR. HOTAIR is an abbreviation for long, non-coding RNA, a part of DNA in humans and other vertebrates. HOTAIR does not produce a protein on its own but, when it is being expressed or functioning, it can suppress genes that would normally slow tumor growth or cause cancer cell death.
High levels of HOTAIR expression have been linked to breast tumors, pancreatic and colorectal cancers, sarcoma and others.
UT Arlington researchers found that when breast cancer and mammary gland cells were exposed to BPA in lab tests, the BPA worked together with naturally present molecules, including estrogen, to create abnormal amounts of HOTAIR expression. Their results were published online in February by the Journal of Steroid Biochemistry and Molecular Biology.
“We can’t immediately say BPA causes cancer growth, but it could well contribute because it is disrupting the genes that defend against that growth,” said Mandal, who is corresponding author on the paper.
“Understanding the developmental impact of these synthetic hormones is an important way to protect ourselves and could be important for treatment,” he said.
Bhan is lead author on the paper. Co-authors include Mandal lab members Imran Hussain and Khairul Ansari, as well as Linda Perrotti, a UT Arlington assistant professor of psychology, and Samara Bobzean, a member of Perrotti’s lab.
“We were surprised to find that BPA not only increased HOTAIR in tumor cells but also in normal breast tissue,” said Bhan. He added further research is needed, but the results beg the question - are BPA and HOTAIR involved in tumor genesis in addition to tumor growth?
BPA has been widely used in plastics, such as food storage containers,