BP‑1‑102 exerts antitumor effects on T‑cell acute lymphoblastic leukemia cells by suppressing the JAK2/STAT3/c‑Myc signaling pathway.

Abstract

Drug resistance and relapse of T-cell acute lymphoblastic leukemia (T-ALL) remain significant concerns for physicians; hence, the development and screening of effective targeted drugs remain important. Considering that STAT3 is emerging as a potential therapeutic target for T-ALL, T-ALL cell lines (MOLT-4 and CUTLL1) were treated with BP-1-102, a small-molecule inhibitor that blocks STAT3 phosphorylation. Cell Counting Kit-8 assay and colony formation assay results showed that BP-1-102 inhibited T-ALL cell proliferation and colony formation. Flow cytometry and morphological results demonstrated that BP-1-102 dramatically induced apoptosis and caused cell cycle arrest at the G0/G1 phase in T-ALL cell lines. Western blotting results indicated that BP-1-102 suppressed the JAK2/STAT3/c-Myc pathway activity in T-ALL cell lines. In conclusion, BP-1-102 suppressed the JAK2/STAT3/c-Myc signaling pathway in T-ALL cells and exerted various antitumor effects, representing a promising targeted antitumor inhibitor.