Lung Cancer Paper Week 3 Draft 3 Part 2

AATF also referred to as, Apoptosis Antagonizing Transcription Factor, is a regulator of p53 in DNA damage response. It is known to inhibit apoptosis in vivo and be overexpressed in lung cancer. In Kras-driven lung adenocarcinoma if the deletion of AATF occurs then this results in delayed lung cancer formation mainly in a p53 dependent manner. Targeting AATF will be targeting tumor progression and putting a stop to it. AATF through the PI3K/Akt pathway can inhibit Ba. This then results in the activation of BCL-2 leading to immortality of these multiplying cells.  We know that BCL-2 works in the survival pathway. Its job is to stop cell death. When a phosphate is added to Bad it could then prevent it from sequestering Bcl₂, so Bcl₂ can do its function. Bad prevents Bcl₂ from doing its job. When Bad is bound to Bcl₂, the cell will die, however, when Bad is not bound to Bcl₂, Bcl₂ will be active and it will stop cell death. In order to keep Bad inactive, protein 14-3-3 will make sure a phosphate is stuck on Bad.