Apoptosis is a physiological response in development and homeostasis of metazoans. Apoptosis is triggered during pathological events as a means to renew affected tissues and eliminate cancer cells. The immune system regulates the extrinsic pathway of apoptosis, where signals such as TNFα or displayed ligands on the surface of immune cells trigger signal cascades by death receptors present on targeted cells.

NOXA is a critical mediator of stress responses to anticancer drugs. This BH3-only protein sets the apoptotic threshold in cancer cells in response to chemotherapies by counteracting the prosurvival BCL-2 family protein MCL-1. A complex and dynamic network relying on both highly controlled gene transcription activity and protein degradation by proteasome, regulates cellular NOXA levels from low in steady state to rapidly enhanced upon stressful condition.

Autophagy was originally viewed as a widely conserved multistep lysosomal degradation pathway in eukaryotes. It includes the formation of autophagosomes, doublemembrane structures engulfing cytoplasm with damaged organelles during the degradation process.

Autophagy is the one of the essential pathways for maintaining homeostasis of cells and plays an important regulatory role in cell survival and death. Tp53-induced glycolysis and apoptosis regulator (TIGAR) is a Tp53 target protein and is not only involved in the regulation of metabolism, cell cycle progression and radiation response, but also plays a role in autophagy.

Alpha-fetoprotein (AFP) is a tumorous marker for the diagnosis of hepatocellular carcinoma (HCC), it is synthesized mainly by the embryo yolk sac, fetal liver and the gastrointestinal tract. AFP belongs to the family of protein products of albuminoid genes, which are located in tandem arrangement in chromosome 4 (region 4q11-q13).