AKR1B10 inhibits the proliferation and metastasis of hepatocellular carcinoma cells by regulating the PI3K/AKT pathway

作者：Ke Tian, Ying Deng, Zhipeng Li, Huaxin Zhou, Hui Yao · 发表于：Oncology Letters · 年份：2023 · DOI：10.3892/ol.2023.14151 · 被引用次数：13 · 研究领域：Aldose Reductase and Taurine、Alcohol Consumption and Health Effects、Heme Oxygenase-1 and Carbon Monoxide

Hepatocellular carcinoma (HCC) is one of the most frequent and aggressive malignant neoplasms, and is associated with a poor prognosis. Therefore, there is a crucial need to develop novel cancer therapies and identify novel therapeutic targets. Aldo-keto reductase family 1 member B10 (AKR1B10) is expressed in various types of cancer. However, the role of AKR1B10 in the pathological process of HCC and its underlying molecular mechanism is poorly understood. AKR1B10 expression was evaluated pan-cancer and in HCC using the Genomic Data Commons-The Cancer Genome Atlas (GDC-TCGA) and International Cancer Genome Consortium (ICGC) databases. The relationship between elevated AKR1B10 expression and overall survival in HCC patients was analyzed using a Kaplan-Meier plot. The effects of AKR1B10 on the proliferation, migration, and invasion of HCC cells were evaluated. The proliferation of HCC was measured using CCK-8 and colony formation assays. Transwell and wound healing assays were used to assess the migration and invasion of HCC cells. Western blots were used to detect the expression of proliferative and epithelial-mesenchymal transition (EMT) related proteins in HCC cells, including CCND1, E-cadherin, N-cadherin, vimentin, Twist1, PI3K/p-PI3K, and AKT/p-AKT. AKR1B10 expression was significantly upregulated pan-cancer and in liver cancer. Upregulated AKR1B10 expression was associated with a worse overall survival. HCC cell proliferation, migration, and invasion were found to be inf...