One of the most striking results obtained in this study following silencing of CSNK2β was a highly significant upregulation of p21 at the transcript level. p21 is well known as sensor and effector of multiple growth inhibiting signals and its overexpression has been reported to cause arrest in breast carcinoma cell lines (Sheikh et al., 1995[ 47 ]).
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Knockdown of CSNK2ß suppresses MDA-MB231 cell growth, induces apoptosis, inhibits migration and invasion.
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