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Tumour Biol. 2016 Oct;37(10):13843-13853. Epub 2016 Aug 2.

Tescalcin expression contributes to invasive and metastatic activity in colorectal cancer.

Kang J1, Kang YH1,2, Oh BM1,3, Uhm TG1, Park SY1,2, Kim TW1,3, Han SR4, Lee SJ1,3, Lee Y1,2, Lee HG5,6.

Author information

1
Genome Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 305-806, South Korea.
2
Department of Biochemistry, College of Natural Sciences, Chungbuk National University, Cheongju, Chungbuk, South Korea.
3
Department of Biomolecular Science, University of Science and Technology (UST), Daejeon, South Korea.
4
Department of Biological Science, Daejeon University, Daejeon, South Korea.
5
Genome Structure Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, 305-806, South Korea. hglee@kribb.re.kr.
6
Department of Biomolecular Science, University of Science and Technology (UST), Daejeon, South Korea. hglee@kribb.re.kr.

Abstract

We reported previously that tescalcin (TESC) levels were higher in tissue and serum from colorectal cancer (CRC) patients and suggested that TESC was a potential oncotarget in CRC. The aim of this study was to investigate the function of TESC in CRC invasion and metastatic potential. TESC expression was knocked down in CRC cells using small interfering RNA (siRNA). The expression of TESC siRNA reduced cell migration and invasion by inhibiting matrix metalloprotease (MMP) and the epithelial-mesenchymal transition (EMT) pathway. RT-PCR and Western blot analysis showed that TESC siRNA induced E-cadherin. Consistently, TESC overexpression in HCT116 (HCT/TESC) cells enhanced cell migration and invasion by activating MMP and the EMT pathway and reducing E-cadherin. The formation of liver metastatic nodules in vivo was strongly increased in mice injected with HCT/TESC cells compared with that in mice injected with HCT/mock cells. This study demonstrates that TESC is involved in cell migration, invasion, and EMT during CRC tumor invasion. These results implicate TESC as a metastatic mediator and provide a biological rationale for the adverse prognosis associated with elevated TESC expression in human CRC.

KEYWORDS:

Colorectal cancer; Epithelial-mesenchymal transition; Invasion; Metastatic mediator; Tescalcin

PMID:
27485112
DOI:
10.1007/s13277-016-5262-0
[Indexed for MEDLINE]

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