LDLRAD2 promotes pancreatic cancer progression through Akt/mTOR signaling pathway

被引:0
|
作者
Junhe Li
Wei Huang
Qing Han
Jianping Xiong
Zhiwang Song
机构
[1] The First Affiliated Hospital of Nanchang University,Department of Oncology
来源
Medical Oncology | 2021年 / 38卷
关键词
LDLRAD2; Pancreatic cancer; EMT; Warburg effect; Akt/mTOR pathway;
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学科分类号
摘要
Low-density lipoprotein receptor class A domain containing 2 (LDLRAD2) acts as a protein-coding gene in a large number of human diseases. However, the potential roles and underlying mechanism in pancreatic cancer remains unclear. Therefore, this study was conducted to address this question. Herein, we found that the expression of LDLRAD2 was elevated in pancreatic cancer tissues and cell lines. LDLRAD2 knockdown inhibited pancreatic cancer cell proliferation, migration, and invasion in vitro. Besides, silencing LDLRAD2 impaired tumor growth and metastasis in vivo and up-regulated the E-Cadherin level, whereas down-regulated the expression of N-Cadherin and Vimentin levels, which indicating that LDLRAD2 knockdown suppresses EMT. Additionally, LDLRAD2 knockdown decreased the Warburg effect and glycolytic enzymes expression. Pathway scan assay and western blotting assay indicated that LDLRAD2 knockdown significantly down-regulated the expression of phosphorylation of Akt and phosphorylation of mTOR, which suggested that knockdown of LDLRAD2 inhibits Akt/mTOR signaling pathway. Taken together, these findings suggested that LDLRAD2 may be an oncogene in pancreatic cancer via modulating Akt/mTOR signaling pathway.
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