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Cancerous melanoma tumors grow and are more likely to metastasize due to interactions between a pair of molecules, based on experiments in mice and human cells. The findings could restore the potential of a type of cancer treatment abandoned previously in clinical trials. The findings also implicate a molecule already linked to obesity and dementia as a potential cause of metastasis, or spread of cancer cells in other parts of the body.
Melanoma is responsible for about 1% of skin cancers, but is responsible for the vast majority of skin cancer deaths, according to the American Cancer Society. There are few treatments to prevent melanoma metastases.
A research team led by Associate Professor Beate Heissig of the Institute of Medical Sciences at the University of Tokyo has studied the tissue-type plasminogen activator (tPA) for more than ten years. TPA is a protease, a small molecule capable of cutting proteins. TPA binds to a larger protein in the membrane barrier of animal cells, called low density lipoprotein receptor (LRP1) protein 1.
The Heissig research team proposes to block the action of tPA by promoting metastasis by preventing it from connecting to LRP1. Mice without LRP1 had smaller tumors, even when the researchers provided additional tPA.
Other studies have associated LRP1 with chronic diseases such as diabetes, obesity, and Alzheimer's disease.
"It is surprising that LRP1 also regulates the growth and spread of cancer.It is normally a receptor for fat molecules," Heissig said.
Controlling the spread of cancer
In 2016, the Heissig research group discovered that mice that received more tPAs had a greater number of a specific type of cells. This same type of cells usually increases in melanoma tumors and can promote tumor growth. Based on this potential connection, the current project was designed to study the role that tPA could play in skin cancer.
When the cancer cells metastasize, they use proteases to cut through the matrix of protein chains that keep the healthy cells in place. When cancer cells enter a new part of the body and start to form new tumors, they corrupt nearby cells to create a niche or support house for themselves.
Clinical researchers have tried to prevent metastases by stopping proteases. However, complete blockage of all proteases causes undesired side effects. No protease-based anticancer treatment has been successful in clinical trials.
"Our vision is an anti-cancer therapy that specifically prevents the interaction of LRP1 and tPA, so that only the metastatic effect of the protease is stopped, healthy actions of tPA proteases," said Yousef Salama , first author of the research paper and postdoctoral researcher in the Heissig laboratory.
Salama also suggests that tPA could be linked to cancer immunotherapy, the life-saving treatment rewarded by the 2018 Nobel Prize in Physiology or Medicine.
"The scientific community knows that tPA can interfere with the cellular signals studied for cancer immunotherapy." The blockage of tPA could enhance the action of the immune system and potentially enhance the effectiveness of the treatments. 39, cancer immunotherapy, "said Salama.
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Material provided by University of Tokyo. Note: Content can be changed for style and length.
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