Abstract
ATP1B3 encodes the β3 subunit of Na+/K+-ATPase and is located in the q22-23 region of chromosome 3. Na+/K+-ATPase participates in normal cellular activities but also plays a crucial role in carcinogenesis. In the present study, we found that expression of the β3 subunit of Na+/K+-ATPase was increased in human gastric cancer tissues compared with that in normal matched tissues and that this increased expression predicted a poor outcome. ATP1B3 expression was elevated at both the mRNA and protein levels in gastric cancer cell lines relative to those in a normal gastric epithelial cell line. Interestingly, ATP1B3 knockdown significantly inhibited cell proliferation, colony-formation ability, migration, and invasion and increased apoptosis in human gastric carcinoma cell lines. Additionally, knockdown induced cell cycle arrest at the G2/M phase. Furthermore, we demonstrated that ATP1B3 silencing decreased the expression of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and phosphorylated AKT (p-AKT), indicating that ATP1B3 regulates gastric cancer cell progression via the PI3K/AKT signalling pathway. Hence, the β3 subunit of Na+/K+-ATPase plays an essential role in the tumourigenesis of gastric cancer and may be a potential prognostic and therapeutic target for the treatment of gastric cancer.
Highlights
Gastric carcinoma is one of the most common malignancies and the third leading cause of cancer-related deaths worldwide [1]
We demonstrated that ATP1B3 silencing decreased the expression of phosphatidylinositol 3-kinase (PI3K), protein kinase B (AKT) and phosphorylated AKT (p-AKT), indicating that ATP1B3 regulates gastric cancer cell progression via the PI3K/AKT signalling pathway
To verify the oncogenic function of the ATP1B3 protein product in gastric cancer, we evaluated its expression in 30 primary gastric cancer tissue samples and matched normal tissue samples by IHC staining
Summary
Gastric carcinoma is one of the most common malignancies and the third leading cause of cancer-related deaths worldwide [1]. According to the cancer control programme of the World Health Organization, 7 million patients die of cancer worldwide each year, and 700,000 of these deaths are due to gastric cancer [2]. Despite improvements in detection and treatment, gastric carcinoma remains one of the most aggressive malignancies, with an extremely poor prognosis, and is a major cause of cancer death worldwide [3]. Elucidation of the molecular mechanisms underlying gastric carcinoma is urgently needed to enhance early diagnosis and cure rates. New treatment approaches, such as targeted knockdown of oncogene expression have been assessed. Identification of critical targets in advanced stomach cancer is needed to develop effective treatments
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