Catchy LKB1 Title

1. Catchy LKB1 Title Liver Kinase B1 (LKB1) in Cancerous Growth Billions of dollars are being poured into the research of cancer, the National Cancer Institute alone spends $4.9 Billion every year. Liver Kinase B1 (LKB1) stands out as one important protein that regulates cell metabolism, cell division, and therefore, cancerous growth. LKB1 is a key regulator of cell metabolism and cell division by acting as a tumor suppressor by turning on other proteins that suppress tumor growth. Human mutations in LKB1 causes the disease Peutz-Jeghers syndrome, which results in benign tumor-like growth called polyps in the intestine and a 50% chance of developing cancer by the age of 50. When cell energy, ATP, is low LKB1 will be activated. Active LKB1 regulates the activity of adenosine monophosphate-activated protein kinase (AMPK). LKB1 directly activates AMPK by adding a phosphate group to Thr-172. AMPK activity increases the production of ATP by activating glycolysis and fatty acid oxidation. AMPK can also decrease the amount of energy needed by the cell by inhibiting protein synthesis and cell growth. Both of these processes play a role in cancer development. Drugs like Metformin, a successful diabetic drug, are thought to activate LKB1. Through the activation of AMPK to cease cancerous growth, and with the whole cascade of proteins ceases cancerous growth. The Grafton SMART (Students Modeling A Research Project) Team modeled LKB1 using #D printing technology. The SMART program is supported by a grant from NIH-CTSA. Explanation of Diagram + + + + + Above is an image of two cells, both with LKB1 mutation resulting in the lack of AMPK phosphorylation. The one with Metformin results in more LKB1 and AMPK interaction and thus AMPK phosphorylation versus the control. Metformin, a popular anti diabetic drug, activates Adenosine-monophosphate Activated Kinase (AMPK) by extracting Live Kinase B1 out from the nucleus and into the cytoplasm where AMPK is generally locates. It does this by phosphorylating LKB1 at Ser428 which then helps LKB1 export from the nucleus and meet with AMPK in the cytoplasm, hence phosphorylating AMPK and continuing the natural cycle. Introduction Cellular polarization, structure, and cell energy balance are all a direct result of Liver Kinase B1's (LKB1) sequence of activation. Cellular polarization occurs when Protease-activated Receptor (PAR1) is phosphorylated by LKB1, which then makes the cell more structurally stable. Adenosine monophosphate-activated protein kinase (AMPK) is also activated by LKB1 which then inhibits cellular energy consumption such as ATP consumption for protein synthesis and turns off anabolic pathways required for cell division. Heterozygous pathogenic mutations in LKB1 inhibit it from phosphorylating PAR1 and AMPK, resulting in the loss of the structural integrity of the cell and also the activation of anabolic pathways which lead the cell to eventually divide. This mutation is evident in patients suffering from Peutz-Jeghers syndrome in which benign polyps are present inside the intestine. Patients with Peutz-Jeghers syndrome are prone to colon and rectal cancers as well as a wide variety of other cancers. Explanation of Diagram + + + + +