Antitumor hepatocytes

Stimulating healthy liver cells to counteract cancer

Alexander Gorlov, XX2 century

In the course of a study conducted at the Cancer Biology Center of the Flemish Institute of Biotechnology (Vlaams Instituut voor Biotechnologie, VIB) and the Catholic University of Leuven (Katholieke Universiteit Leuven), together with employees of a number of other research organizations, scientists found that healthy liver tissue surrounding a cancerous tumor activates a protective mechanism that prevents the development of cancer. It is noteworthy that, as experiments with mice have shown, hyperactivation of this mechanism, that is, its activation above the levels usual for the liver, triggers the process of elimination of various types of its tumors in it. This discovery outlines the contours of a new strategy for combating cancer of this organ and may lead to the development of new therapeutic methods for mobilizing normal cells to destroy cancer cells. The results of the study are published in the journal Science (Moya et al., Peritumoral activation of the Hippo pathway effects YAP and TAZ suppresses liver cancer in mice).

Fight against tumors

Modern forms of chemotherapy are aimed at destroying rapidly multiplying cancer cells. However, such treatments often do not work for long, because cancer cells quickly become resistant to drugs. Currently, other approaches are being used, such as immunotherapy, the purpose of which, instead of directly affecting tumor cells, is to activate the natural protective function of the immune system.

The above-mentioned study, conducted under the leadership of Professor Georg Halder, showed that not only the immune system, but also non-malignant liver cells around the tumors formed in it are capable of killing tumor cells. When experimentally activated in mice with liver tumors of this newly discovered mechanism, the life expectancy of experimental animals increased significantly, and tumors decreased sharply.

"Although," notes Professor Halder, "this antitumor mechanism, as our study has shown, exists, but it is not known exactly how activated liver cells cause cancer cells to eliminate, and this is obviously a very important issue, and we are working on it now."

Unexpected genes

By studying tumor tissues in cancer patients and mouse models suffering from liver cancer, the researchers found that the YAP and TAZ genes are activated around tumors of this organ and that this is the main driving force of the antitumor mechanism.

This observation caused surprise, because usually in various human oncological diseases there is a high expression of YAP and TAZ, leading to the reproduction and survival of tumor cells. "The detection of antitumor functions in genes whose activity has traditionally been considered to contribute to the development of tumors completely changes our understanding of cancer–causing genes and their functions in normal tissues," states Ivan Moya, lead author of the article presenting the results of this study.

To new methods of treatment

Although the study showed that the detected antitumor mechanism can kill tumors and metastases in the liver, it is not yet known whether activation of similar mechanisms occurs in other organs. "Since we were able to discover the amazing antitumor effect of the liver cells activated by the YAP gene on its tumors, our discovery can stimulate the emergence of amazing ideas about a new control strategy," says Stephanie Castaldo, another lead author of this article.

Although a remarkable discovery has been made in experiments with mice, in the light of which a completely new strategy for fighting cancer is emerging, the researchers have given only a primary description at the molecular level for the antitumor mechanism they have just discovered, and, therefore, additional research is needed to study how the results obtained can be applied to the treatment of cancer in humans. "Of course, the next step is to find out to what extent this mechanism also works in the case of human cancer cells," notes Laura Van den Mooter, the third lead author of the scientific article.

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