Original Paper

Journal of Cancer Research and Clinical Oncology

, Volume 135, Issue 6, pp 761-769

Upregulation of the cycline kinase subunit CKS2 increases cell proliferation rate in gastric cancer

  • Min Ah KangAffiliated withStem Cell Research Center, Korea Research Institute of Bioscience and Biotechnology
  • , Jong-Tae KimAffiliated withStem Cell Research Center, Korea Research Institute of Bioscience and Biotechnology
  • , Joo Heon KimAffiliated withDepartment of Pathology and Preventive Medicine, Eulji University School of Medicine
  • , Soo-Young KimAffiliated withDepartment of Pathology and Preventive Medicine, Eulji University School of Medicine
  • , Young Ho KimAffiliated withDepartment of Internal Medicine, Samsung Medical Center
  • , Young Il YeomAffiliated withStem Cell Research Center, Korea Research Institute of Bioscience and Biotechnology
  • , Younghee LeeAffiliated withDepartment of Biochemistry, Chungbuk National University
  • , Hee Gu LeeAffiliated withStem Cell Research Center, Korea Research Institute of Bioscience and Biotechnology Email author 

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Abstract

Purpose

CKS2 was identified as an upregulated gene in gastric cancer via our DNA microarray. This study was to verify the upregulation of CKS2 in many gastric cancer patients and to examine the CKS2-mediated cellular response.

Methods

CKS2 upregulation was analyzed using reverse transcriptase PCR, real-time PCR, and immunohistochemical and clinicopathological analyses. GFP-CKS2 or CKS2-siRNA was used to analyze the cellular localization and proliferation.

Results

The strong upregulation of mRNA and protein levels of CKS2 was identified. In CKS2-overexpressing cells, tumor suppressor p53 and p21cip1 were downregulated and cell growth was increased. In contrast, CKS2-siRNA-transfected cells showed an increased tumor suppressor expression and decreased cell growth.

Conclusions

We showed that CKS2 was significantly upregulated in gastric cancers and a high level of CKS2 was highly correlated with histologic tumor differentiation and pathological grade of the tumor size, lymph node, and metastasis stage. We suggest that the cell cycle regulator CKS2 might be deeply involved in gastric cancer progression.

Keywords

CKS2 CDK1 p53 Gastric cancer