Abstract
Proline-rich protein 11 (PRR11) together with its upstream adjacent gene, spindle and kinetochore associated 2 (SKA2), represent a classic, head-to-head gene pair. The role of the PRR11 and SKA2 gene pair has been described in various types of cancer, including breast cancer, non-small cell lung cancer, hepatocellular carcinoma and ovarian carcinoma. However, its role in esophageal carcinoma (ESCC) remains unclear. The mRNA expression levels of PRR11 and SKA2 were examined in ESCC surgical specimens. In addition, the role of PRR11 and SKA2 in the proliferation and migratory and invasive capacities of EC9706 and EC109 cell lines was examined. The results from the present study demonstrated that PRR11 and SKA2 expression levels were upregulated in ESCC tissues compared with adjacent normal tissues. Furthermore, PRRl1 and SKA2 knockdown significantly inhibited the proliferation and migratory and invasive capacities of ESCC cells. Conversely, PRRl1 and SKA2 overexpression significantly promoted the proliferation and migratory and invasive capacities of ESCC cell lines via activation of the AKT signaling pathway and certain markers of epithelial-mesenchymal transition, including Snail and N-cadherin. The results from the present study suggested that the PRR11 and SKA2 gene pair may represent a potential target in the diagnosis and treatment of ESCC.
Highlights
Esophageal squamous cell carcinoma (ESCC), which is one of the most common types of cancer, was the sixth leading cause of cancer‐associated mortality in China in 2016 [1]
The results demonstrated that PRR11 expression level was significantly increased in ESCC tissues compared with the adjacent normal tissues (P
To identify the function of the PRR11 and spindle and kinetochore associated 2 (SKA2) gene pair in ESCC cells, specific shRNA targeting PRR11 and/or SKA2 were used in EC9706 cells
Summary
Esophageal squamous cell carcinoma (ESCC), which is one of the most common types of cancer, was the sixth leading cause of cancer‐associated mortality in China in 2016 [1]. Based on previous epidemiologic studies, it is widely accepted that genetics serve a crucial role in the development and progression of ESCC [4,5]; the underlying mechanisms remain unclear. PRR11 has been reported to serve as a candidate oncogene in various types of cancer, including pancreatic cancer, breast cancer, non‐small cell lung cancer, hepatocellular carcinoma and ovarian carcinoma [7,8,9]. Studies on PRR11 and SKA2 mainly focus on lung and breast cancer [7,8,10]; the role of PRR11 and SKA2 in ESCC remains unclear
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