I found a ‘bad protein’ that makes cancer cells proliferate… Anticipating the development of new cancer drugs
The research team of Professor Seo Joon-young of Yonsei University
Test of biperine metabolism control function, etc.
| Joon-Young Seo is a professor in the Department of Biomedical Sciences, Yonsei University College of Medicine. /Photo courtesy of Yonsei University |
The regulatory mechanism of innate immunity-derived proteins that promote the proliferation, growth and survival of cancer cells has been identified. As a result, the development of new anticancer therapies is expected.
A research team led by Professor Joon-Young Seo of the Department of Biomedical Sciences, College of Medicine, Yonsei University College of Medicine recently announced that they had identified the cancer metabolism control function and mechanism of action of biperine, a interferon-expressed protein known to cause antitumor immunity. The results of this study were published in the latest issue of the International Journal of Clinical Research.
In the process of tumor tissue formation, tumor cells, unlike normal cells, have the characteristic of changing metabolism so that they can proliferate, grow, metastasize and survive even under adverse conditions such as nutrient deficiency and limited oxygen.
The research team investigated the cancer metabolism control function and mechanism of action of ‘viperin’, one of the interferon-inducing proteins.
First, the research team confirmed that biperine expression was elevated in various types of tumor tissue. Biperine expression was elevated in tumor tissues of stomach cancer (288 cases), lung cancer (230 cases), breast cancer (1981 cases), kidney cancer (443 cases), pancreatic cancer (184 cases) and patients with brain cancer (206 cases). The higher the number, the lower the survival rate of cancer patients.
To confirm the metabolic control function of biperine in cancer cells, the research team created and tested cancer cell lines that suppressed or strongly expressed biperine.
As a result of the analysis, it was found that the expression of biperine was induced not only by interferon, but also by oxygen starvation and nutrient starvation in the cancer microenvironment, promoting energy metabolism and fatty acid synthesis in cancer cells, allowing cancer cells to proliferate and survive.
In particular, it was confirmed that biperine is expressed in cancer stem cells resistant to anticancer drugs and can differentiate into various cancer cells, promoting metabolic changes and improving the characteristics of cancer stem cells. This function of biperine was confirmed to promote tumor growth in experimental mouse xenograft models.
Professor Joon-Young Seo said: ‘We have identified a novel mechanism in which the protein biferin, which is expressed by interferon known to cause anti-cancer immunity, regulates cancer stem cells and cancer cell metabolism to promote the proliferation, growth and survival of cancer”. Through this, it is anticipated that it will be possible to overcome the limitations of existing cancer treatments and develop treatments that target cancer metabolism.”
Editor Jang Ik-kyung
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