Isoliquiritigenin attenuates tumor progression and PD-L1 expression by inhibiting the phosphorylation of STAT3 in melanoma.

Abstract

Isoliquiritigenin (ISL) has been reported with antitumor activities. While, the underlying molecular mechanisms remain largely unknown. The transcription factor of programmed cell death ligand 1 (PD-L1), STAT3, plays an important role in tumor metastasis. In this study, we first verified that ISL suppressed the growth and metastasis ability of melanoma cells both in vitro and in vivo. Then, we found that ISL could repress the expression of PD-L1 and STAT3 phosphorylation. TIMER algorithm analysis showed that the levels of immune infiltration were positively correlated with the expression of STAT3. Furthermore, the STAT3 phosphorylation inhibitor Stattic could enhance the effect of ISL in suppressing cell proliferation, promoting apoptosis, and restraining the ability of migration and invasion of melanoma cells. This study revealed that ISL inhibited melanoma metastasis and repressed PD-L1 expression by repressing the phosphorylation of STAT3, which help us to understand the mechanism of ISL in melanoma therapy.