A groundbreaking discovery by USC researchers has revealed a new and unexpected mechanism of how cancer cells spread. The study focused on the protein GRP78, which was found to move to the nucleus of stressed cancer cells, altering gene activities and promoting the cells’ mobility and invasiveness. This surprising finding has significant implications for cancer treatment strategies and offers new possibilities for therapeutic approaches.
The research, funded by the National Institutes of Health and led by Dr. Amy S. Lee, involved investigating how GRP78 regulates the gene EGFR, known for its association with cancer. To their amazement, the researchers discovered that GRP78 not only controls EGFR gene activity but also enters the nucleus of cells, a location previously thought to be its primary residence in the endoplasmic reticulum.
Further examination using advanced imaging techniques confirmed the presence of GRP78 in the nucleus of lung cancer cells, as well as normal cells under stress. The researchers found that when GRP78 is in the nucleus, it stimulates the activity of genes related to cell migration and invasion. This unexpected function of GRP78 results from its binding to another cellular protein called ID2, which usually suppresses genes involved in cell migration. However, when bound to GRP78, ID2 loses its ability to suppress these genes, leading to increased invasiveness in cancer cells.
The implications of this discovery are far-reaching. It opens up potential avenues for cancer treatment, such as targeting GRP78 to suppress EGFR in lung cancer or blocking its interaction with ID2. Additionally, the finding may revolutionize the understanding of cell biology, suggesting that other proteins could also change their function and behavior by relocating within the cell under stress or other triggers.
Dr. Lee and her team are exploring drugs that can inhibit GRP78’s expression or activity, potentially leading to new therapeutic strategies. The study’s results have been published in the Proceedings of the National Academy of Sciences and offer a promising step forward in the fight against cancer.
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Frequently Asked Questions (FAQs) about cancer cell spread
What did the USC researchers discover?
The USC researchers discovered a new and unexpected mechanism of cancer cell spread. They found that the protein GRP78 migrates to a cell’s nucleus under stress, altering gene activities and promoting cancer cells’ mobility and invasiveness.
What are the implications of this discovery?
The discovery has significant implications for cancer treatment strategies. It offers new possibilities for developing therapeutic approaches to target the protein GRP78 and prevent cancer cell invasiveness.
What role does GRP78 play in cancer cells under stress?
Under stress, GRP78 gets hijacked in cancer cells, allowing viral invaders to replicate and making the cancer cells more resistant to treatment. The protein’s movement to the nucleus leads to changes in gene activities and increased mobility in cancer cells.
How was the discovery made?
The discovery was made using advanced imaging techniques, such as confocal microscopy, to directly observe GRP78 in the nucleus of lung cancer cells. The researchers also used RNA sequencing and other biochemical analyses to understand the genes affected by GRP78’s presence in the nucleus.
What are the potential new approaches for cancer treatment?
The study suggests several potential new approaches for cancer treatment, including down-regulating the activity of GRP78 to suppress EGFR in lung cancer or preventing GRP78 from binding to ID2, another cellular protein that promotes cell migration and invasion.
Does GRP78 play a role in other types of cancer?
Yes, GRP78 plays a similar role in various types of cancers, including pancreatic, breast, and colon cancer. This discovery has broad implications for cancer research across different cancer types.
Who funded the research?
The research was funded by the National Institutes of Health (NIH), supporting the investigation into the role of GRP78 in cancer cell spread.
Is there ongoing research on inhibiting GRP78 activity?
Yes, Dr. Amy S. Lee and her team are studying drugs that can inhibit the expression or activity of GRP78. Preliminary studies suggest that small molecules inhibiting GRP78 may block its activity in the nucleus of cells, providing a potential avenue for cancer treatment.
More about cancer cell spread
- Surprising Finding: Scientists Discover New, Unexpected Mechanism of Cancer Cell Spread
- Proceedings of the National Academy of Sciences: ER chaperone GRP78/BiP translocates to the nucleus under stress and acts as a transcriptional regulator
- Keck School of Medicine of USC
- National Institutes of Health (NIH)
1 comment
ths could chnge evrythin! now we got new leads 4 cancer treatment! bravo Keck School of Med! gonna read that study! NIH is rockin!