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Research Paper|Volume 15, Issue 18|pp 9661—9675

Aberrant expression of AKR1B1 indicates poor prognosis and promotes gastric cancer progression by regulating the AKT-mTOR pathway

Luojie Liu1, Lihua Zhu1, Zhengwu Cheng2, Yibin Sun3, Yuqing Zhou3, Jiwei Cao4
  • 1Department of Gastroenterology, Changshu Hospital Affiliated to Soochow University, Suzhou 215501, China
  • 2Department of Gastrointestinal Surgery, The First Affiliated Hospital of Wannan Medical College, Wuhu 241000, China
  • 3Department of Gastroenterology, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu 215005, China
  • 4Department of General Surgery, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Suzhou, Jiangsu 215005, China
* Equal contribution
Received: May 23, 2023Accepted: August 21, 2023Published: September 24, 2023
https://doi.org/10.18632/aging.205041

Copyright: © 2023 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Gastric cancer (GC) is a common malignant tumor in the digestive tract and a major cause of global cancer death. Due to the limited access to early screening, many patients are diagnosed with advanced GC. Therefore, postoperative radiotherapy and chemotherapy possess limited efficacy in treating GC. AKR1B1 has been associated with tumorigenesis and metastasis across various tumors, becoming a potential therapeutic target for GC. However, its role and mechanism in GC remain unclear. In this study, AKR1B1 was elevated in GC tissue, depicting a poor prognosis. AKR1B1 is closely related to age, vascular and neural invasion, lymph node metastasis, and the TNM stage of GC. The developed survival prediction model suggested that AKR1B1 expression level is crucial in the prognosis of GC patients. Moreover, the expression level of AKR1B1 in GC tissues is closely associated with the AKT-mTOR pathway. In vitro and in vivo assays functional assays helped determine the oncogenic role of AKR1B1. Additionally, the knockdown of AKR1B1 expression level in GC cell lines could effectively suppress the AKT-mTOR pathway and inhibit the proliferation and migration of tumor cells. In conclusion, this study provides a theoretical basis to establish the potential association and regulatory mechanism of AKR1B1 while offering a new strategy for GC-targeted therapy.