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.

中文翻译：

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BP-1-102 通过抑制 JAK2/STAT3/c-Myc 信号通路对 T 细胞急性淋巴细胞白血病细胞发挥抗肿瘤作用。

T 细胞急性淋巴细胞白血病 (T-ALL) 的耐药性和复发仍然是医生的重要关注点；因此，开发和筛选有效的靶向药物仍然很重要。考虑到 STAT3 正在成为 T-ALL 的潜在治疗靶点，T-ALL 细胞系（MOLT-4 和 CUTLL1）用 BP-1-102（一种阻断 STAT3 磷酸化的小分子抑制剂）处理。Cell Counting Kit-8检测和集落形成检测结果显示BP-1-102抑制T-ALL细胞增殖和集落形成。流式细胞术和形态学结果表明，BP-1-102 显着诱导细胞凋亡并导致细胞周期停滞在 G ₀ /G ₁T-ALL 细胞系中的阶段。蛋白质印迹结果表明 BP-1-102 抑制了 T-ALL 细胞系中的 JAK2/STAT3/c-Myc 通路活性。总之，BP-1-102通过抑制T-ALL细胞中的JAK2/STAT3/c-Myc信号通路发挥多种抗肿瘤作用，是一种很有前景的靶向抗肿瘤抑制剂。