STAT3 and neoplasm: However, the influence of SOCS3 in these processes may be mediated, in part by a prominent role of STAT3 activation in the tumor cells, as the decrease in cell proliferation and invasion in vitro by overexpression of SOCS3 was less marked in a cell line (OSCC3) in which a biochemical STAT3 inhibitor was also less effective; other mechanisms may be compensating for the inhibitory function of SOCS3 and of the biochemical inhibitor on STAT3 activation, such as let-7a microRNA which contributes to constitutive STAT3 phosphorylation in malignant cholangiocytes [32].