For a long time thinking about cutting cellular cell metabolism to prevent cancer, the protein complex AMPK seems to increase tumors and help acute researchers. Now, Salk Institute researchers have solved a long secret around why AMPK could interfere with and help cancer.
Laboratory Salk Professor Reuben Shaw has shown that late-stage cancer can cause AMPK's cellular recycling signal cannibalize pieces of the piece, supplying large lung tumors with nutrients they need to grow. The work that appeared Cell metabolism On November 8, 2018, it is suggested that in some cases the blocking of AMPK will help increase the lung cancer's most common tumor.
"Our research shows that the same dysfunction in the genetic circle initiating lung cancer in the cell is essential for the survival of tumor cells when they have enough nutrients," says Shock, director of the Salk of Cancer Center and the author of the newspaper. "It's exciting, because not only does it turn into genetically" Voodoo ", but it also indicates a potential new therapeutic goal of cancer that is often diagnosed with diagnosis.
AMPK operates as a fuel gauge cell, supervising energy input and output maintenance to keep running smoothly. As well as a car sensor, low frequency signal or energy saving energy, AMPK exceeds cell growth and changes cell metabolism if the cell fuels (nutrients) are low. Earlier, Shomma found that AMPK could reduce tumor metabolism and restore normal function in liver and other tissues with diabetes.
But the new work of the show's laboratory suggests that AMPK actually helps to develop large tumors. In the current study, the team is observed from mice groups and AMPK without fuels to develop tumors.
"We found that the tumor was increasing more slowly when the AMPK was not present," says Lillian Eichner, a research fellow at the newspaper. "This means that AMPK does not always function as tough as hard as we initially thought."
The team analyzed which of the mouse tumor cells were activated in different conditions. One gene that was particularly active was Tfe3, which is known to activate cellular processing. It was found that when the tumors were sufficiently sufficient to use nutrients, the AMPK TF3 started processing cigarette materials as nutrients – for effectively using cell tissue – the tumor.
"We were previously focused on how we could be activated by AMPK," says Eichner. "Now that we have seen this mechanism, we can move on to some cancer."
The show, chaired by William R Brood, adds: "We're excited because advanced tumors seem to help AMPK to have this mechanism that we can treat them."
Other authors were Sonia N. Bruni, Sevastien Herzig, Nathan Yong, Stephanie D. Kurtis, David B. Shaklord, Maxim N. Shakiraev, Matthias Lelbani, Liliana I Vera, Amanda Huchin, Sisters S. Rossi and Robert W. Svenson
The work was funded by the National Institutes of Health (R35CA220538, P01CA120964), Samuel Waxman Cancer Research Foundation, Leon M. And Harry B. Helsilis Charity Fund (Grant # 2012-PG-MED002) and American Cancer Society (ACS) # 124183-PF-13-023-01-CSM) (PF-15-037-01-DMC).
Materials provided Salk Institute. Note: Edit content for style and length.