According to the American Daily Science Network, researchers at the Stanford-Burnham Institute of Medicine have discovered an enzyme called PKCzeta that can inhibit the formation of prostate tumors and has been confirmed in experimental mice and humans. In addition, the study also described a molecular pathway that controls tumor cell growth and metastasis. The researchers said this discovery is a major advancement in the treatment of prostate cancer and will help scientists develop new ways to control tumor progression. Related papers were published in the "Journal of the National Academy of Sciences" recently.
The research was done in collaboration with the laboratory of Dr. Maria Diaz-Mick and Dr. George Moscat. They found that PKCzeta can control the gene expression of the tumor-prone gene c-Myc. Normally, PKCzeta can keep the expression of c-Myc under monitoring, but the researchers found that in prostate cancer and other cancer patients, the level of PKCzeta is low, which makes c-Myc enhance the cancer cell Growth and transfer.
Previous studies have shown that PKCzeta is a possible tumor suppressor, but its role in prostate cancer has been a mystery. In the new study, the team used genetically engineered mice that had completely lost the PKCzeta enzyme to analyze their effects.
Dias-Mick said: "In this study, we evaluated the role of PKCzeta in prostate cancer, and for the first time demonstrated the tumor suppressor function of mice without the PKCzeta gene. But I think that The biggest takeaway from this research is the discovery of the way PKCzeta works in prostate cancer. "
The researchers found in the experiment that PKCzeta cooperates with the PTEN gene to achieve the function of suppressing tumors. They knew that PTEN is a tumor suppressor long ago, and they also knew its variant form in prostate cancer. But if only the normal function of PTEN is lost, it will not cause malignant prostate cancer. This study finally solved the mystery that puzzled scientists, confirming that the lack of PKCzeta and the excessive activation of c-Myc caused by it are the main causes of malignant prostate cancer.
This discovery portrays two potential therapies against prostate cancer: gene therapy to activate PKCzeta factor or its downstream molecules in prostate cancer, or the development of a method that can inhibit c-Myc activity in the absence of PKCzeta drug.
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