National Yang-Ming University and Taipei Veterans General Hospital recently unveiled a breakthrough finding that explains how cancer cells promote the recruitment of tumor-associated macrophages to remodel a tumor’s microenvironment to aid growth.
The research team was led by Yang Muh-hwa (楊慕華), a professor in the university’s Institute of Clinical Medicine and an attending physician at the hospital’s Division of Hematology-Oncology, who discovered that a protein that gives cells the abilities to migrate from their original locations and to invade blood or lymph vessels — or other organs — also changes the behavior of white blood cells.
Drosophila embryonic protein SNAI1 — known as Snail — a transcriptional repressor protein that induces epithelial-mesenchymal transition (EMT), can also modulate the tumor microenvironment to turn macrophage white blood cells into allies, the researchers found.
“The formation of a malignant tumor requires both the seed, which is cancer cells, and soil, which is host cells, such as immune cells, vascular endothelial cells and fibroblasts. Hence, how the tumor cells manage to bypass the monitoring of the host’s immune system and transform ‘soldiers’ defending against their invasion into their helpers has been a key factor in the aggravation of cancer tumors,” Yang said.
With the assistance of the school’s Institute of Microbiology and Immunology associate professor Chen Nien-jung (陳念榮) and the hospital’s Department of Otorhinolaryngology, Head and Neck Surgery physician Tai Shyh-kuan (戴世光), Yang found that when a tumor is slightly inflamed, the tumor necrosis factor alpha (TNFα) — a regulator of white blood cells — that it produces facilitates a protein transformation called the acetylation of Snail.
“Our team subsequently discovered that acetylated Snail is able to attract the host’s macrophages to assemble around tumor cells,” Yang said.
Furthermore, the team members observed that almost all the white blood cells lured into the tumor are M2 macrophages, Yang said, which suppress inflammation and encourage tissue repair, allowing tumor cells to grow and proliferate.
Yang said that in addition to M2 macrophages, another major subset of human macrophages are M1 macrophages, which encourage inflammation and mount defenses against foreign pathogens and would otherwise inhibit tumor growth.
“As acetylated Snail cannot only attract M2 macrophages, but also transform M1 macrophages near the tumor into M2 type, it plays a key role in creating a supportive and nourishing microenvironment for tumor growth,” Yang said.
Medical specialists have focused primarily on eliminating cancer through chemotherapy, but few have explored treating cancer by blocking the communication between cancerous cells and immune system cells, which could create an inhospitable environment for cancer growth, he said.
Yang said as the team’s research primarily targeted patients with head and neck cancers, his next objective is to find out whether the above form of communication also exists between human immune system cells and other cancers.
“We also plan to determine which types of cancer patients might be suitable for a ‘communication-blocking’ treatment and whether the TNFα inhibitors used to treat rheumatic diseases can also help obstruct the communication,” he added.
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