MiR-216b inhibits gastric cancer proliferation and migration by targeting PARK7.

Abstract

Postoperative recurrence and metastasis of gastric cancer is still a difficult problem in medical field. About 60% of patients with advanced gastric cancer die from peritoneal metastasis, which has become one of the main causes of death of gastric cancer patients. To elucidate the molecular mechanism of peritoneal metastasis of gastric cancer can help us better early diagnosis and improve treatment measures. This project intends to validate the above hypothesis from three different levels of tissue, cell, and animal models by means of fluorescence quantitative PCR, Western blot, double Luciferase Report Analysis and immunohistochemical detection, and to further explore the molecular mechanism of peritoneal metastasis of gastric cancer. Our previous studies have shown that PARK7 promotes peritoneal metastasis of gastric cancer through PI3K/Akt signaling pathway, but its specific regulatory mechanism remains unclear. Our preliminary study showed that the expression of microRNA-216b in gastric cancer tissues with peritoneal metastasis was significantly lower than that in patients without peritoneal metastasis, while the expression of PARK7 was the opposite.