Tao Wang, Fan Shi, JiQuan Wang, Zi Liu, Jin Su
Oncology Research, Vol.28, No.9, pp. 969-970, 2020, DOI:10.3727/096504022X16414984936773
Abstract Kallistatin has been recognized as an endogenous angiogenesis inhibitor and exerts pleiotropic effects in inhibiting tumor growth, migration, apoptosis, and inflammation. The purpose of the present study was to investigate the potential role and mechanisms of kallistatin in cervical cancer. We demonstrated that kallistatin
effectively inhibited cell proliferation and enhanced apoptosis in a dose-dependent manner. Additionally, kallistatin suppressed migration and invasion activities and markedly reduced the expression of matrix-degrading
metalloproteinases, progelatinase (MMP-2), MMP-9, and urokinase-type PA (uPA). Kallistatin reversed the
epithelial–mesenchymal transition (EMT) and caused the upregulation of epithelial markers such as E-cadherin
and inhibited mesenchymal markers such as N-cadherin… More >
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