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When administered, and after reaching the cancer cells, the insulin stimulates their replication and also switches them in to receiving mode

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Towards this end, we used HeLa cells in which endogenous PDS5B is silenced by an siRNA targeting the 3-UTR of the PDS5B mRNA and complemented with an ectopically expressed, siRNA resistant form of HA-tagged PDS5B WT or PDS5B 17A