LKB1 is regulated by p53 in response to glucose deprivation

다국어 초록 (Multilingual Abstract)

The tumor suppressor LKB1 is an evolutionarily conserved serine/theronine kinase. In humans, LKB1 can be inactivated either by germ line mutations resulting in Peutz-Jeghers syndrome or by somatic mutations causing predisposition to multiple sporadic cancers. LKB1 has wide-ranging functions involved in tumor suppression and cell homeostasis, including establishing cell polarity, setting energy metabolic balance (via phosphorylation of AMP-dependent kinase), regulating the cell cycle, and promoting apoptosis. LKB1 function was previously linked to the tumor suppressor p53 and shown to activate the p53 target gene p21/WAF1. To investigate correlation between p53 and LKB1, we used HEK293, HCT116 p53 WT and Null cell line. In this study, we show that protein levels of LKB1 in HCT116 p53 null cells are more down-regulated than them of HCT116 p53 WT Cells by glucose deprivation. Here, the protein levels of LKB1were increased over-expression of p53 WT. Also, the LKB1 mRNA levels were increased by over-expression of p53 WT but not p53 DN(dominant negative). Therefore, these results indicate that the p53 is positive regulator of LKB1 in glucose deprivation.

목차 (Table of Contents)

• Abstract 1
• Introduction 2
• Experimental Procedure 4
• Results 6
• Discussion 9
• Figure Legends 10
• Figures 13
• Reference 18