PWP1 Affects Gastric Cancer Progression by Regulating p53 and JAK1 and Its Expression in Gastric Cancer.

Background：Gastric cancer is a globally important disease and the fifth most diagnosed malignant cancer in the world. Because it is usually diagnosed at an advanced stage, gastric cancer has a high mortality rate, making it the third most common cause of cancer-related death. Hot spots of gastric cancer incidence and mortality exist in East Asia, Eastern Europe and South America. It is still an urgent problem to find new diagnostic and prognostic markers and better understand the molecular mechanism of gastric cancer. Although radical resection and systemic chemotherapy have shown great improvement, the prognosis of gastric cancer (GC) patients is still depressing due to malignant proliferation and metastasis. Therefore, it is urgent to clarify the potential molecular mechanism of gastric cancer progression, which will contribute to the development of targeted therapy. Effective induction of tumor cell apoptosis is the most important feature of a new chemical agent for cancer treatment. There is increasing evidence that the cell cycle can act in concert with apoptosis to cause cell death under certain cellular stress conditions. A comprehensive understanding of the relationship between apoptosis and cell cycle is essential for developing effective cancer therapies.

PWP1 is also known as endonuclein, which contains five WD40 repeated domains and belongs to the WD40-repeated superfamily. It is highly expressed in human pancreatic adenocarcinoma, where it functions as a cell-cycle regulator. However, the normal function of Pwp1 is largely unknown. Previous research data show that PWP1 plays a key role in regulating biological functions such as RNA processing, signal transduction, gene expression, vesicle transport, cytoskeleton assembly and cell cycle progression. Whether the high expression of PWP1 is ubiquitous in tumors, the relationship between the high expression and clinicopathological factors of tumors, and the mechanism of PWP1 in tumors are still unclear. Further exploration of the molecular mechanism of PWP1 in GC may provide new ideas and therapeutic targets for GC treatment in the future, and benefit clinical patients.