Tescalcin expression contributes to invasive and metastatic activity in colorectal cancer

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Tescalcin expression contributes to invasive and metastatic activity in colorectal cancer
Jieun Kang; Yun Hee Kang; Byung Moo Oh; Tae Gi Eom; Sang Yoon Park; Tae Woo Kim; S R Han; Seon-Jin Lee; Yonghee Lee; Hee Gu Lee
Bibliographic Citation
Tumor Biology, vol. 37, no. 10, pp. 13843-13853
Publication Year
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.
Colorectal cancerEpithelial-mesenchymal transitionInvasionMetastatic mediatorTescalcin
Springer Verlag (Germany)
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Division of Research on National Challenges > Environmental diseases research center > 1. Journal Articles
Division of Biomedical Research > Immunotherapy Research Center > 1. Journal Articles
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