Protein kinase C delta (PKC delta), a subtype of PKC family, has been recognized as a tumor promoter or suppressor depending on different tissue specificities in various tumor types. However, the effects of PKC delta on somatotropinomas are poorly understood. This study aims to explore the precise role of PKC delta in promoting tumor progression in somatotropinomas. In the present study, we examined the expression levels of PKCd in clinical specimens of human somatotropinomas to show that PKCd overexpression correlated with invasive properties of somatotropinomas. Furthermore, we employed rat anterior pituitary GH3 cells as the experiment model to demonstrate that PKC delta activation by PKC agonist (Phorbol-12-myristate-13-acetate, PMA) significantly promoted the proliferation and migration potential of GH3 cells, and these effects could be abolished following PKCd inhibition by specific inhibitor Rottlerin. Mechanistically, PKC delta activated ERK1/2 signaling, which was responsible for PKC delta-induced promotion of GH3 cell proliferation and migration. Taken together, our results indicated that PKCd functions as a tumor promoter by promoting cell proliferation and migration in somatotropinomas.