Further MTT assays showed a trend that growth of PRKCI -amplified cell lines is greatly inhibited by knockdown of PKCι whereas silencing PKCι displayed little effect in growth of non- PRKCI -amplified lines (Fig. 3d ).
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Addiction to protein kinase Cɩ due to PRKCI gene amplification can be exploited for an aptamer-based targeted therapy in ovarian cancer.
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