本研究旨在通过靶向miR-21调节JAK2/STAT3信号通路，研究DUSP1对宫颈癌（CC）细胞的影响。为此，从2021年1月至2023年2月在我院接受治疗的15例CC患者中选取病理组织和癌旁组织，通过Western blot和qPCR检测DUSP1蛋白和mRNA的表达水平。建立了C33a对照组（COG）和DUSP1过表达组（OVG）：C33a COG中的人宫颈鳞癌细胞（CSCC）在无任何处理的情况下培养，而DUSP1 OVG则使用DUSP1基因过表达的慢病毒感染后代培养。通过CCK8测定了三组细胞的增殖能力，通过Western blot和qPCR检测了蛋白和mRNA的表达，通过Transwell测定了细胞的迁移和侵袭能力。结果发现，CC组织中的DUSP1蛋白和mRNA的表达水平较PC组织低（P<0.05）。DUSP1 OVG中的miR-21较C33a COG中的miR-21降低（P<0.05）。DUSP1 OVG中的JAK2、STAT3 mRNA和蛋白的表达水平较C33a COG中下降（P<0.05）。总之，DUSP1的过表达可以靶向并降低miR-21的表达，阻断JAK2/STAT3信号通路，降低CC细胞的活力，抑制CC细胞的增殖、迁移和侵袭能力，并诱导CC细胞凋亡，从而为临床CC的靶向治疗提供理论依据。

This study was to investigate the effect of DUSP1 on cervical cancer (CC) cells by targeting the miR-21 regulatory JAK2/STAT3 signaling pathway. For this purpose, fifteen CC patients treated at our hospital from January 2021 to February 2023 were selected. CC tissues and para-cancerous (PC) tissues were collected from the patients, and DUSP1 protein and mRNA expression levels were detected by Western blot and qPCR. The C33a control group (COG) and DUSP1 overexpression group (OVG) were set up: human cervical squamous carcinoma cells (CSCC) in the C33a COG were cultured without any treatment, while the DUSP1 OVG was cultured using DUSP1 gene overexpression lentivirus infection progeny. The proliferation ability of the three groups of cells was measured by CCK8, protein and mRNA expression by Western blot and qPCR, and cell migration and invasion ability by Transwell. It was found that DUSP1 protein and mRNA in CC tissues were reduced compared with those in PC tissues (P<0.05). The miR-21 in the DUSP1 OVG was reduced than those in the C33a COG (P<0.05). The expression of JAK2, STAT3 mRNA and protein in the DUSP1 OVG were reduced compared with those in the C33a COG (P<0.05). In conclusion, overexpression of DUSP1 can target and reduce the expression of miR-21, block the JAK2/STAT3 signaling pathway, reduce the viability of CC cells, inhibit the proliferation and migration and invasion ability of CC cells, and induce apoptosis of CC cells, thus providing a theoretical basis for the targeted treatment of clinical CC.