Figure 4

Proposed effects of calcitonin and MAP kinase pathways on CD44 expression in androgen-independent prostate cancer. Calcitonin (CT) binds to its receptor (CTR), which is coupled to the G_sα transduction protein. G_sα activity, mediated through cAMP, activates protein kinase A (PKA) [19, 25]. PKA activates the MAPK kinase (MEK)-extracellular regulated kinase (ERK) pathway, that facilitates CD44 transcription. CT also induces splicing of CD44 to include v7-10, dependent on p38 but not on PKA. p38 may be induced by Exchange protein activated by cAMP (Epac). p38 could affect splicing machinery directly, through other downstream effectors, or by causing release of intracellular Ca²⁺.