Hormel Institute Scientists Make Discovery That Could Lead to New Treatments for Lung Cancer

A team of scientists from The Hormel Institute, University of Minnesota, led by Luke Hoeppner, PhD, Associate Professor and leader of the Cancer Biology research section, has published research that could lead to new treatments for lung cancer.

Lung cancer is the deadliest and most common type of cancer worldwide. It is responsible for 1.8 million deaths each year. Non-small cell lung cancer (NSCLC) is the most common type of lung cancer, accounting for 85% of cases. The five-year survival rate for NSCLC patients is poor because the disease can become resistant to treatment and it often spreads to other parts of the body.

Overexpression is when too many copies of a protein or other substance occurs. It can play a role in cancer development. A protein called IKKα is overexpressed in lung cancer and elevation of IKKα is tied to poor survival rates for lung cancer patients. Dr. Hoeppner and his team previously found that IKKa promotes lung tumor cell migration when it interacts with another protein called DARPP-32. The findings from this study show that IKKa activates DARPP-32. DARPP-32 can then control protein phosphatase 1 (PP1) activity,
which can stimulate cancer-causing molecules and pathways.

The study was primarily funded by a Research Scholar Grant from the American Cancer Society. Dr. Hoeppner also received funding from The Elsa U. Pardee Foundation and from the Wildfeldt Cancer Research Award, a community-supported internal pilot project grant.  Community-funded pilot studies like the Windfeldt Cancer Research Award are essential for scientists to develop early ideas to the point where they compete successfully for larger grants.

This research was led by Sk. Kayum Alam, PhD, a Senior Scientist in Dr. Hoeppner’s research
group. Dr. Hoeppner’s team also included Li Wang, PhD, and Zhu Zhu, a former visiting
scholar.

The article, “IKKα promotes lung adenocarcinoma growth through ERK signaling activation via
DARPP-32-mediated inhibition of PP1 activity” was published in the journal Precision
Oncology.