Overexpression of TYRO3 indicates poor prognosis and induces gastric cancer progression via AKT-mTOR pathway

Gastric cancer (GC) is among of the leading causes of cancer mortality worldwide. This is because many patients are diagnosed with advanced GC and postoperative radiotherapy and chemotherapy have also exhibited limited effects on GC. TYRO3 has been considered carcinogenic and a potential therapeutic target for GC. However, TYRO3 function and mechanism in GC remains elusive. The study results indicated that TYRO3 was aberrantly elevated in GC tissues and predicted poor prognosis. TYRO3 is closely associated with clinicopathological indicators in GC tissues such as lymph node metastasis, venous invasion, neural invasion, and the tumor-node-metastasis stage. In addition, TYRO3 expression levels are closely related to the AKT-mTOR pathway in GC tissues. Moreover, the oncogenic role of TYRO3 was determined through in vitro and in vivo functional assays, and knockdown of the TYRO3 expression level in GC cell lines can effectively suppress the AKT-mTOR pathway and inhibit tumor cell proliferation and migration. In conclusion, this study provides a theoretical basis for establishing the potential association and regulatory mechanism between TYRO3 and AKT-mTOR and offers a new strategy for GC-targeted therapy.

Automated summary

Gastric cancer is a leading cause of cancer deaths worldwide. TYRO3 has been identified as a potential therapeutic target for GC as its expression is increased in GC tissues and is associated with poor prognosis, clinicopathological indicators, and the AKT-mTOR pathway. Functional assays showed that TYRO3 plays an oncogenic role by activating the AKT-mTOR pathway, and knocking down TYRO3 can inhibit tumor cell proliferation and migration. This study provides a theoretical basis for the potential association between TYRO3 and AKT-mTOR and offers a new strategy for GC-targeted therapy.