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      How does Cancer Spread in the Body | Answer Inside

      Researchers from the University of Southern California (USC) have unveiled important insights into how cancer cells metastasize, offering potential new strategies to stop their spread. 

      The research, by the National Institutes of Health, focuses on a cellular chaperone protein known as GRP78, which regulates the folding of other proteins within cells.

      Researchers team at the Keck School of Medicine of USC had previously found that when cells are under stress, GRP78 is commandeered, enabling viral invaders to replicate and cancers to grow and resist treatment. 

      So, their latest findings reveal an unexpected twist in the tale of this protein’s role in cancer progression.

      GRP78 resides in the endoplasmic reticulum, a part of the cell.

      But under stress, it migrates to the cell’s nucleus, altering gene activities and changing the cell’s behaviour, thereby enabling cancer cells to become more mobile and invasive. 

      This observation of GRP78 controlling gene expression in the nucleus was describe by Dr Amy S Lee as a novel phenomenon in the basic mechanisms of cancer cells.

      The discovery began incidentally when Ze Liu, a postdoctoral researcher in Lee’s lab, was analysing how GRP78 regulates a gene known as EGFR, long associate with cancer. 

      Dr Amy S Lee notice that GRP78 controls the gene activity of EGFR, suggesting that GRP78 may have enter the nucleus and assume a new role. 

      To confirm this, the team use high-resolution imaging techniques to directly observe GRP78 in the nucleus of lung cancer cells and normal cells under stress.

      Investigation reveal that key genes regulate by GRP78 in the nucleus are mainly involve with cell migration and invasion.

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      The Researchers team found that GRP78 binds to ID2, another cellular protein that typically suppresses genes allowing cells to migrate. 

      When bound to GRP78, ID2 can no longer suppress these genes, leading to increase invasiveness of cancer cells.

      These findings suggest potential new approaches for cancer treatment, such as down-regulating the activity of GPR78 to suppress EGFR in lung cancer or preventing it from binding to ID2. 

      This discovery also opens up a new line of research in cancer biology, as GRP78 plays a similar role in various types of cancers, including pancreatic, breast, and colon cancer.

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