Found Breast Cancer Metastasis and Suppressor Cells... UNIST Researchers "Cancer Cells Can Be Controlled"
Professor Ji-Young Park's Team Reveals Function of Adipocytes in Tumor Microenvironment
Regulation of FAM3C Secretome → Control of Cancer Cells, Opening Path for Diagnosis and Treatment
Cells that directly inhibit the metastasis of breast cancer have been discovered.
These cells, which directly regulate the growth and metastasis of breast cancer, are expected to be applied in various fields including early diagnosis and drug development for breast cancer.
UNIST (President Yong-Hoon Lee) announced on the 4th that Professor Ji-Young Park’s team from the Department of Life Sciences has revealed for the first time that ‘cancer-associated adipocytes’ in the tumor microenvironment of breast cancer regulate the survival and metastasis of breast cancer cells.
Adipocytes present in the tumor microenvironment, which refers to the cellular environment where the tumor exists, can provide energy supply necessary for cancer cell growth and various secretions that promote proliferation.
Cancer cells alter the characteristics of these adipocytes to activate such functions, and these altered adipocytes are called cancer-associated adipocytes.
A schematic of a study showing that in the cancer-associated adipose tissue (sWAT) of a breast cancer mouse model, inhibition of FAM3C leads to increased adipocyte apoptosis (CC3) and fibrosis (Fibronectin, Sirius Red).
View original imageThe research team discovered that cancer-associated adipocytes found in the breast cancer tumor microenvironment regulate a secretory factor called FAM3C. They confirmed for the first time in the world that this regulated secretory factor induces changes in the breast cancer tumor microenvironment, promoting the survival and metastasis of nearby breast cancer cells.
Professor Ji-Young Park said, “When the secretion of FAM3C increases in the early stages of breast cancer, the survival of cancer-associated adipocytes increases and fibrosis is suppressed. When fibrosis, which causes hardening of part of an organ, is suppressed, various secretions can easily access cancer cells, promoting their survival and growth.”
Conversely, in the late stages of breast cancer, cancer-associated adipocytes reduce the expression of the FAM3C secretory factor. Unlike in the early stages, they promote fibrosis of the cancer-associated adipocytes.
Cancer-associated adipocytes that occur in the late stages of cancer change the tumor microenvironment to become more rigid through fibrosis. This change makes it easier for cancer cells to move and invade, thereby promoting cancer metastasis.
The research team experimentally demonstrated the process of inhibiting cancer cells. They confirmed that inhibiting the FAM3C secretory factor of cancer-associated adipocytes in the early stages of breast cancer suppresses the growth and metastasis of breast cancer.
Professor Ji-Young Park (third from the right in the front row) and Researcher Sa-Hee Kim (second from the right in the back row).
View original imageProfessor Ji-Young Park of the Department of Life Sciences stated, “We have verified that cancer-associated adipocytes directly regulate the growth and metastasis of breast cancer through the secretory factor FAM3C. We expect our experimental results to be utilized in future research on early diagnostic markers and metastatic treatment development for breast cancer.”
First author Researcher Sa-Hee Kim said, “This study will present a new perspective on early diagnosis and metastasis inhibition of breast cancer through the secretory factor FAM3C of cancer-associated adipocytes.”
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The results of this study were published online on December 20, 2023, in Cancer Research, a top international journal in the field of oncology published by the American Association for Cancer Research. The research was conducted with support from the Ministry of Science and ICT and the National Research Foundation of Korea (Bio·Medical Technology Development Project, Individual Basic Mid-Career Research Project, Leading Research Center).
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