New target protein linked to regulation, movement of tumor-associated macrophages

New target protein linked to regulation, movement of tumor-associated macrophages

Developing a therapy to combat cancer remains one of the most difficult challenges in medical research. Cancer owes its notorious identity to the fact that the cancer cells use the host's own immune system to grow and spread, ultimately becoming deadly. Immune cells like macrophages, which ordinarily fight to protect normal cells, are hijacked by malignant cancer cells, and populate the environment around the tumors, becoming tumor-associated macrophages (TAMs). In fact, it was found that the cancerous tissue of patients for whom immunotherapy was not successful was indeed rich in macrophages, confirming the link between the cancer and the TAMs. It is these TAMs that produce signaling proteins like chemokines and trigger the inhibitory immune checkpoint releases that create an immunosuppressive tumor environment, which protects the cancer cells and allows their accelerated growth. Since it is the TAMs that facilitate the spreading of cancer cells, regulating them as a therapeutic strategy for combating cancer has gained attention in recent years. A research group led by Yuya Terashima from the Tokyo University of Science saw this as an opportunity to explore the realm of developing novel anti-cancer drugs. Their seminal work in Nature Immunology 2005 reported the discovery of a new target protein called FROUNT, which is linked to regulation and movement of the TAMs. Since FROUNT amplified "chemokine signaling," a type of cellular communication, an integral process for TAM accumulation and activity, it was therefore linked directly to TAM regulation. The team decided to expand on these findings, in order to investigate whether a therapeutic strategy can be formulated and have published their findings in Nature Communications . Through animal experiments, the researchers found that by regulating FROUNT expression in TAMs, cancer growth could be suppressed. Related Stories



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