Non-Cell-Autonomous Tumor Suppression by p53
Introduction and significance for the entire manuscript (Guide: approx one quarter page/150 words).
The p53 is a vital tumour suppressor protein in humans which is important for cell cycle regulation. Ablation of the p53 protein causes the cell to proliferate infinitely that contributes to the development of tumours. Through the cell-autonomous program the cell-cycle arrest and apoptosis is caused by the presence of p53. The aim of the journal is to study cellular senescence program in hepatic stellate cells that is p53-dependent which is formed by dying hepatocytes which secret factors that influence the tissue microenvironment, preventing fibrosis, cirrhosis and liver cancer via promoting p53 senescent in these HSCs. The research objectives explain that fibrosis is limited through the p53-mediated senescence program by stopping HSC proliferation through cell-autonomous canonical senescence regulators and the non-cell-autonomous effects of SASP on ECM and immune surveillance. Currently there is a debate on the role p53 plays in HSCs which influences later stages of liver cancer and the research exhibits that through non-cell-autonomous mechanisms, p53 can inhibit cancer by manipulating the tissue microenvironment.
Key Figure (Guide: approx one half page/400 words).
Figure 5 is the key figure in this journal. Figure 5 justifies the macrophage function and polarization how it’s influenced by SASP program that is driven by