Most pancreatic cancer cells have a mutation in the KRAS gene and can proliferate in a disorderly manner. In this image, the carcinogenic version of the KRAS protein is stained red in pancreatic cancer cells. KRAS outlines the plasma membrane, which is the outer layer of the cell. The cell nucleus is dyed blue. Researchers at the Cold Spring Harbor Laboratory have discovered a new mechanism that may explain how pancreatic cancer cells develop resistance to drug therapies that target the KRAS protein. Credits: Derek Cheng / Tuveson lab / CSHL
Cancer cells can be resistant to adaptive treatment and are notorious for being difficult to defeat and are extremely deadly. David Tuveson, director of the Cold Spring Harbor Laboratory (CSHL) Cancer Center, and his team investigated the basis of “adaptive resistance” common to pancreatic cancer. They found one of the backups in which these cells switch when faced with a drug that kills cancer.
KRAS is the driving gene Cell division.. Most pancreatic cancers have mutations in the KRAS protein that cause uncontrolled growth. However, drugs that block mutant KRAS do not stop growth. cancer cell Find a way to avoid blockages and continue to divide. Derek Cheng, the lead author of the study and a student of Tuveson Lab’s former medical scientist training program, compares this process to a ship’s backup engine. Main engine, I’m using some kind of backup engine. But it overcame them. The ship hasn’t sunk yet. It’s still moving at a slow pace. Ultimately what we want to do is sink the ship. “”
Tuveson and his team wanted to understand these “backup engines.” cancer cell. They used a technique called biotin proximity labeling to identify which other proteins interacted with mutant KRAS. “I basically attach the spray can to my favorite protein, in this case the protein I hate the most. So I attach biotin and basically spray biotin onto nearby proteins. And I can analyze it. Know which proteins are labeled: “”
As seen in these pancreatic cells, proteins do not promote cell division when KRAS (red) is modified to stay in the cytoplasm or center of the cell. In pancreatic cancer cells, KRAS mutants stay near the outer layer of the cell and interact with nearby proteins to divide the cell too much. Credits: Derek Cheng / Tuveson lab / CSHL, 2021
Scientists Discovered “Biotin Paint” protein The name RSK1 is part of a complex that keeps nearby protein groups dormant called the RAS protein. Scientists were surprised that inactivating mutant KRAS also caused the nearby RSK1 complex to fail. This activated the RAS protein and allowed it to take over the function of the missing mutant KRAS.
Stop Pancreatic cancer Cells may need drugs that can target multiple molecules at the same time. Tubeson wants to reveal many players who are contributing to the adaptation of cancer cells to improve future treatments.
Derek K. Cheng et al, carcinogenic KRAS, is involved in the RSK1 / NF1 pathway and inhibits wild-type RAS signaling in pancreatic cancer. Minutes of the National Academy of Sciences (2021). DOI: 10.1073 / pnas.2016904118
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Cold Spring Harbor Laboratory
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