Cell Death Linked to Tumor Growth in Prostate Cancer Patients

Source: University of Michigan

Summary: In a new study, researchers have found the reason why the body’s own immune system helps cancer to spread in prostate cancer metastasis.

The aim of any cancer treatment is to kill cancer cells. Yet, one little-understood paradox of certain cancers is that the body’s natural process for removing dead and dying cells can actually fuel tumor growth. Prostate cancer (cancer in man’s prostate gland), in its final stages often spreads to the bone; at this point, it can no longer be cured because the environment helps a speedy tumor growth. In fact, 65-80% of the cases of prostate cancer metastasis occurs in the bone. In a new study, researchers from the University of Michigan have found the reason why the body’s own immune system helps cancer to spread especially in prostate cancer metastasis. The research findings were published in The Journal Clinical Investigation.

A pro-inflammatory protein - CXCL5 induces tumor growth

Model of efferocytosis-induced prostate cancer tumor growth in the bone microenvironment. Credit: University of Michigan/JCI

The process of removing cellular debris is called efferocytosis, which is an important and natural function in healthy individuals and those with cancer. These cellular house cleaners are called as phagocytes. The study was done in mouse models and the researchers found that with metastatic prostate cancer cells, efferocytosis produced a pro-inflammatory protein – CXCL5. This CXL5 protein is not released during cellular cleanup in healthy situations. It was also found that CXL5 protein stimulates tumor growth. However, when the CXCL5 protein was blocked in mice, tumor progression was inhibited. Since bone is a rich pool of the phagocytic immune cells, these findings shed light on the tumor growth paradox which can lead to novel effective cancer therapies.

Lead author, Hernan Roca said, “In the presence of cancer, uncontrolled cell growth is also accompanied by a high, or significant, amount of cancer cell death,” and those dead cells must be removed, and further added,  “The challenge for the future is to understand how to treat these patients to avoid this pro-inflammatory and tumor promoting response, while still preserving the essential function of cell removal.”

More Information: Hernan Roca et al, “Apoptosis-induced CXCL5 accelerates inflammation and growth of prostate tumor metastases in bone”, Journal of Clinical Investigation (2017). DOI: 10.1172/JCI92466


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