信号转导和转录激活因子3 (STAT3) 在淋巴瘤中发现是持续激活的，调节多个致癌过程，因此被认为有潜力作为治疗靶点。本文我们构建了一种抗CD19-N-(4-羧基环己甲基)马来酰亚胺-N-羟基琥珀酰亚胺酯 (SMCC)-前列脱素 (CSP)-STAT3 小干扰 RNA(siRNA) 结合物，并证明 CSP-STAT3 siRNA 结合物能在体外特异结合正常 B 细胞和 A20 淋巴瘤细胞。它减少了 B 细胞淋巴瘤细胞系(A20, SU-DHL-2 和 OCI-Ly3) 中 STAT3 的表达，导致淋巴瘤细胞的较低 S 期和较高细胞凋亡特征。使用 A20 移植性淋巴瘤模型，我们发现 CSP-STAT3 siRNA 结合物显著抑制了肿瘤的生长和重量。在 CSP-STAT3 siRNA 处理的 A20 携带小鼠中，Ki-67, p-STAT3, STAT3 和血清 IL-6 水平明显降低。这些发现表明特异性靶向 B 细胞淋巴瘤细胞系的 STAT3 siRNA 可以显著降低 STAT3 活性并抑制体内外肿瘤的进展，表明其在癌症治疗中的潜在应用。

The signal transducer and activator of transcription 3 (STAT3), which regulates multiple oncogenic processes, has been found to be constitutively activated in lymphoma, suggesting its potential as a therapeutic target. Here, we constructed an anti-CD19-N-(4-carboxycyclohexylmethyl) maleimide N-hydroxysuccinimide ester (SMCC)-protamine (CSP)-STAT3 small interfering RNA (siRNA) conjugate and demonstrated that the CSP-STAT3 siRNA conjugate could specifically bind to normal B cells and A20 lymphoma cells in vitro. It decreased the STAT3 expression in B cell lymphoma cell lines (A20, SU-DHL-2 and OCI-Ly3), resulting in reduced proliferation of lymphoma cells featured with lower S-phase and higher apoptosis. Using an A20 transplantable lymphoma model, we found that the CSP-STAT3 siRNA conjugate significantly inhibited tumor growth and weight. Ki-67, p-STAT3, STAT3, and serum IL-6 levels were all significantly reduced in A20-bearing mice treated with CSP-STAT3 siRNA. These findings indicate that specifically targeting STAT3 siRNA to B cell lymphoma cell lines can significantly decrease STAT3 activity and inhibit tumor progression in vitro and in vivo, suggesting its potential utilization for cancer treatment.