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During hormone responsive (HR) conditions, AR and RON exert a mutually inhibitory effect. We speculate that in the absence of AR or under conditions of androgen deprivation, RON translocates to nucleus and transcriptionally upregulates sub-set of AR target genes including c-FLIP to inhibit apoptosis and promote cell survival; influences EMT process by activating ZEB-2 and reducing E-cadherin. All of these events could contribute to progression to CRPC.
