New potential therapeutic targets for pancreatic cancer


An online study published in the journal Nature has shown that researchers at the University of Texas MD Anderson Cancer Center have developed state-of-the-art methods to track how proteins on the surface of pancreatic cancer cells rearrange. The discovery revealed a protein called SDC1 (syndecan-1) that moves to the cell surface based on signals from KRAS mutants.

The KRAS mutant is a protein known to be present in more than 90% of pancreatic ductal adenocarcinomas. The team believes that a detailed understanding of how KRAS mutations re-prioritize cell membrane function will reveal key new details of the survival pathways of pancreatic cancer cells. Therefore, the researchers designed a method to study the cell surface in a pancreatic cancer model where KRAS can be turned on and off.

The cell surface or "surface body" is dynamic and the cell membrane moves with signals from the cell and the external environment. In cancer cells, cells are preferentially chosen to support their uncontrolled growth due to genetic mutations.

Although the KRAS mutant has been shown to activate pancreatic cancer, the molecular mechanism of this process remains a mystery.

The researchers found that protein on the cell surface changes significantly with KRAS expression, and SDC1 is one of the most abundant proteins in KRAS expression. This is the first direct evidence that KRAS has instructed SDC1 to cross the cell to complete its work on the surface. By using different methods to prevent SDC1 from integrating into the cell membrane, the researchers confirmed that even though SDC1 may be present in the cell, it is only upregulated when it is transferred to the cell surface.

The team provided evidence that SDC1 responds to KRAS signaling and accumulates and induces this pathway on the cell surface. It is further explained that the localization of SDC1 on the cell surface is crucial for the pancreatic cancer cells to up-regulate large-cell drink. Large-cell drink is a mechanism for cells to clear resources into energy or prepare for cell division.

Despite understanding the importance of KRAS in maintaining the survival of pancreatic cancer cells, researchers have encountered difficulties in targeting KRAS. There is currently no clinical drug that completely blocks the KRAS signal, thereby killing cancer cells. Understanding that SDC1 provides energy to pancreatic cancer cells under the control of KRAS may allow tumors with this invasive mutation to be treated by targeting SDC1, and the presence of SDC1 on the cell surface may make it more susceptible to therapeutic intervention.

Researchers believe that the cell surface is an exciting place to find more clues about the fundamental difference between cancer cells and normal cells. Currently, monoclonal antibodies against SDC1 are testing multiple myeloma, a scientific step that may open up clinical studies for similar treatments for pancreatic cancer.
 
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