U-M Research Suggests Studies of a Key Tumor Suppressor Protein Need a Second Look
Study: Commercially available antibodies used to investigate modification of key cancer braking mechanism aren’t fully reliable
At a cellular level, the growth of cancer requires both a foot on the gas pedal of aggressive growth and a removal of vital braking mechanisms.
However, more than 100 studies worldwide involving an abnormal modification in a key braking mechanism — the tumor suppressor protein PP2A — likely need a second look, research led by the University of Michigan Rogel Cancer Center has found.
That’s because a new study, published in Cell Reports, suggests that commercially available antibodies used to investigate the modification aren’t fully reliable.
“Our approach was: Trust but verify,” says senior study author Goutham Narla, M.D., Ph.D., chief of the Division of Genetic Medicine in the Department of Internal Medicine at the U-M Medical School. “And we found these commercially available antibodies were not able to differentiate between the phosphorylated and unphosphorylated forms of this key tumor suppressor protein.”
Narla is collaborating with Egon Ogris, M.D., of the Medical University of Vienna, to commercialize an antibody that specifically detects other key modifications to PP2A stemming from this research for use as a prognostic and/or predictive cancer biomarker.
Paper cited: “Challenges and reinterpretation of antibody-based research on phosphorylation of Tyr307 on PP2Ac,” Cell Reports. DOI: 10.1016/j.celrep.2020.02.012