Cornell scientists released a study Wednesday that could have far-reaching implications for future breast cancer research.
The scientists worked with a type of breast cancer cell that spreads easily to other sites in the body. Until recently, the cell’s pattern of growth had gone unexplained, according to Prof. Michael King, biomedical engineering. “[The cell] originally came from a human breast cancer,” King said. “It’s a good model for the real metastatic disease — if you inject it into mice, they will form tumors all over.” MDA-MB-231 has frustrated researchers because they do not understand why it does not have the ability to adhere to other cells that it would need to spread.For this reason, biomedical engineers are perplexed by it, according to Yue Geng grad. “Everybody thought it wasn’t a good cell line to use [when researching cell adhesion],” Geng said. However, a study published by King and Geng — along with co-authors Jong-Wei Hsu grad, Siddarth Chandrasekaran grad, Andrew Hughes grad and Mishka Gidwani ’15 — concluded that it is not impossible to find a weak spot in these cancer cells.The scientists, Geng said, discovered that “the [MDA-MB-231] cells weren’t in [proper] physiological condition.” By using a drug called Metformin that prevents inflamation and is commonly used to treat type 2 diabetes, the scientists found that Metformin blocks IL-6, a molecule found in the body, interfering with the metastasis of breast cancer cells as well, according to Geng. Over two years ago, when the project began, Geng and her colleague, Hughes, observed how the cancer cells acted in blood plasma, as opposed to in tumors — the first step in understanding how MDA-MB-231 cell adhesion works. “It’s understood that cancer spreads through bloodstream,” King said. “What people don’t understand is how cancer cells change when they enter the blood.”King said that the research the team conducted led them to discover how the cells change when they interact with blood.“We found that these tumor cells switch and act differently when they’re exposed to the different chemicals in the blood. They become more adhesive and grow,” King said.When the cancer cells grow, the cells interact with IL-6, and produce their own IL-6, entering a “positive feedback loop” that ultimately makes the cancer more likely to spread, according to King.The effect is compounded by the fact that breast cancer patients already have more IL-6 in their blood than healthy people. Geng says that it is already widely known that inflammation and cancer are related, but she hopes the study’s focus on cell adhesion will prompt further research on how inflammation connects to cancer cell adhesion.Ultimately, she said, she hopes the research will help fight the spread of breast cancer cells in the body. “All cancer researchers should join forces and better the way we culture in the lab so that we can find out the cancer’s real behavior,” Geng said. Though he says there is much more research to be conducted, King said he believes that the team’s discoveries have the potential to influence how cancer treatments are studied, especially for other cancers that spread through the bloodstream. “In theory, this same signaling behavior and three-dimensional growth could also be true in prostate, colon and skin cancer. … That’s something we’re actively trying to understand,” King said. “This is an area we will continue to study for years to come.”
Original Author: Noah Rankin