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Scientists Analyzing the Molecular Mechanisms of Tumor Suppressor Protein Promoting Cancer

Researchers have long believed that by slowing down cell metabolism, cancer can be effectively suppressed, and protein complex AMPK seems to be able to help some tumors grow. Recently, scientists from Solk Institute have uncovered why AMPK cannot only hinder the progress of cancer, but also help the progress of cancer. Relevant research has been published on internationally magazine Cell Metabolism.

Researcher Reuben Shaw said that advanced cancer can induce AMPK cells to recycle signals and dismantle cell fragments to provide the necessary nutrients for the growth of larger lung tumors. Relevant studies have shown that in some cases, blocking the function of AMPK can inhibit the growth of malignant tumors in common lung cancers. When cancer cells do not need adequate nutrition, the same abnormalities in the genetic circuits that promote the development of non-small cell lung cancer are critical for the maturation of cancer cells. Researchers are thrilled by the results, which not only provide scientists with an understanding of the genetic mystery of cancer, but also provide potential targets for the development of new cancer therapies.

Scientists Analyzing the Molecular Mechanisms of Tumor Suppressor Protein Promoting Cancer

AMPK can act as a cell's "fuel meter", which monitors the input and output of energy to ensure the normal operation of cells. It is similar to automotive sensors, which constantly flicker low gas signals or turn off the alternating current of automobiles to save energy. AMPK also slows down cell growth and changes cell metabolic patterns at low energy levels. Previously, researchers have found that AMPK may slow down the rapid metabolic process of tumors and restore normal functions of liver and other tissues in diabetic patients.

In this study, researchers found that AMPK actually helped large tumors grow. Researchers studied mice carrying AMPK and mice without AMPK to observe the development of tumors in mice. Professor Lillian Eichner said that when AMPK was absent, tumors grew very slowly, which meant that AMPK does not always function as a tumor suppressor.

The researchers then analyzed which genes were activated in tumour cells from the same mouse model in a variety of situations, one of which was Tfe3, which was particularly active and activated the cell recovery process. The results have showed that when the tumour become large enough, it would make the cells in the middle of the tumour become difficult to get nourishment. When nutrients are obtained, AMPK sends a signal to Tfe3 to initiate the recovery of cellular substances such as nutrients for use by tumors. Previously, researchers focused on how to activate AMPK effectively. Now researchers have identified the molecular mechanisms involved, so that researchers can effectively switch to studying how to inhibit AMPK in specific cancers.

Finally, the researcher William R. Brody Chair adds that we are very excited because many malignant tumors seem to rely on AMPK to survive, and understanding the molecular mechanisms involved may provide new ideas for developing new therapies for these malignant tumors.



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