STAT3β is a tumor suppressor in acute myeloid leukemia.

摘要: Signal transducer and activator of transcription 3 (STAT3) exists in 2 alternatively spliced isoforms, STAT3α STAT3β. Although truncated STAT3β was originally postulated to act as a dominant-negative form STAT3α, it has been shown have various STAT3α-independent regulatory functions. Recently, gained attention powerful antitumorigenic molecule cancer. Deregulated STAT3 signaling is often found acute myeloid leukemia (AML); however, the role AML remains elusive. Therefore, we analyzed STAT3β/α messenger RNA (mRNA) expression ratio patients, where observed that higher mRNA correlated with favorable prognosis increased overall survival. To gain better understanding function AML, engineered transgenic mouse allowing for balanced Stat3β expression. Transgenic resulted decelerated disease progression extended survival PTEN- MLL-AF9-dependent models. Our findings further suggest depends on tumor-intrinsic regulation small set significantly up- downregulated genes, identified via sequencing. In conclusion, demonstrate plays an essential tumor-suppressive AML.