MentallyHealth.Org

Over-activation of single gene promotes leukemia, but its loss causes liver cancer

October 06, 2017

"The liver is a most critical metabolic organ in mammals, including humans," said Feng. "It has a unique regenerative capacity that allows it to resist damage by food toxins, viruses and alcohol. Shp2 normally acts to protect hepatocytes. Removing Shp2 from these liver cells leads to their death, which in turn triggers compensatory regeneration and inflammatory responses. That results in enhanced development of HCC induced by a chemical carcinogen."

Feng said the findings highlight the unique mechanism underlying HCC, but more broadly, they reveal new complexities in how different types of cancer begin. Indeed, the researchers say their work also uncovered pro- and anti-oncogenic activities in a gene transcription factor called Stat3.

"Our results indicate a requirement for Stat3 in promoting HCC development, which is consistent with the literature saying Stat3 is pro-oncogenic. But we also found that deletion of Stat3 in hepatocytes resulted in a modest, but significant, increase in HCC."

Feng said the findings underscore the need for caution in designing therapeutic strategies for treating HCCs and other types of cancers because the answer might also be the problem.

Source: University of California - San Diego