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Cancer Manag Res. 2019 Feb 19;11:1717-1723. doi: 10.2147/CMAR.S176771. eCollection 2019.

C14orf159 suppresses gastric cancer cells' invasion and proliferation by inactivating ERK signaling.

Author information

Department of Pathology, Cancer Hospital of China Medical University, Liaoning Cancer Hospital and Institute, Shenyang, Liaoning 110042, P.R. China,
Department of Pathology, People's Hospital of Dawa District, Panjin, Liaoning 124200, P.R. China.
Department of Pathology, Central Hospital of Pulandian District, Dalian, Liaoning 116200, P.R. China.



C14orf159, a new protein, has been identified recently. But its expression in tissues and clinicopathologic correlation is still unknown.

Patients and methods:

We carried out immunohistochemistry staining in 144 gastric cancer cases in this study. Then Western blot was used to detect the expression of protein. MTT and matrigel invasion assay were used to assess the biological effects.


The immunohistochemical results indicated that the expression of C14orf159 in normal gastric mucosa close to cancer tissue was remarkably higher than that in stomach carcinoma samples (63.9% and 34.7%, respectively, P<0.001). Negative C14orf159 expression was dramatically related to high TNM stages (P=0.033) and positive lymph node metastasis (P=0.008). Once C14orf159 was overexpressed, the expression levels of phosphorylated ERK and its regulated downstream molecules, such as Snail, phosphorylated P90RSK and Cyclin D1, were decreased, while the expression level of E-cadherin was increased. Finally, the invasion and proliferation capacity of gastric cancer cells was inhibited.


In other words, loss of C14orf159 is associated with the progression of gastric cancer. The role of C14orf159 in repression of proliferation and invasion may be due to resuming E-cadherin and abolishing Snail and Cyclin D1 expression through inactivating ERK-P90RSK pathway.


C14orf159; ERK; gastric cancer; invasion; proliferation

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