本研究旨在探讨SH2D3A在宫颈癌中的作用，以及其与人乳头瘤病毒（HPV）E7和微小RNA（miRNA）的潜在相互作用。采用定量逆转录聚合酶链反应（qRT-PCR）和免疫组化方法比较SH2D3A 在组织中的表达。为了评估 SH2D3A 对宫颈癌细胞表型的影响，在 SiHa 和 HeLa 细胞中敲低 SH2D3A，然后进行细胞增殖（Cell Counting Kit-8 测定）、细胞凋亡（流式细胞术）和侵袭（Transwell 测定）分析。建立移植瘤模型，比较SH2D3A沉默前后宫颈癌细胞的致瘤能力。生物信息学分析预测和双荧光素酶报告基因检测验证了SH2D3A对miRNA的海绵吸附作用。通过Western blot和qRT-PCR分析HPV E7和SH2D3A下调后对靶基因的影响。宫颈癌组织中SH2D3A表达显着升高。 SH2D3A 沉默可抑制裸鼠细胞增殖和侵袭、诱导细胞凋亡并减少肿瘤发生。生物信息学工具确定了 SH2D3A 和 miR-143-3p 之间的结合关系，并通过荧光素酶报告基因检测证实。蛋白质印迹分析显示，SH2D3A 敲低导致 Janus 激酶 1 (JAK1) 和信号转导子和转录激活子 3 (STAT3) 蛋白的水平降低。此外，qRT-PCR显示HPV E7沉默后SH2D3A mRNA水平下降，而miR-143-3p水平显着升高。HPV E7通过miR-143-3p影响SH2D3A表达，从而调节JAK1/STAT3通路。这一机制促进了宫颈癌的发生和发展。© 2025。亚洲妇科肿瘤学会、韩国妇科肿瘤学会、日本妇科肿瘤学会。

This study aims to explore the role of SH2D3A in cervical cancer, as well as its potential interaction with human papillomavirus (HPV) E7 and microRNA (miRNA).Quantitative reverse transcription polymerase chain reaction (qRT-PCR) and immunohistochemistry were used to compare the expressions of SH2D3A in tissues. To assess the effects of SH2D3A on cervical cancer cell phenotypes, SH2D3A was knocked down in SiHa and HeLa cells, followed by cell proliferation (Cell Counting Kit-8 assay), apoptosis (flow cytometry), and invasion (Transwell assay) analyses. A transplantation tumor model was established to compare the tumorigenic ability of cervical cancer cells before and after SH2D3A silencing. Bioinformatics analysis predicted and dual-luciferase reporter assays verified the sponge adsorption effect of SH2D3A on miRNA. Western blot and qRT-PCR analyses were conducted to examine the impact on target genes following the downregulation of HPV E7 and SH2D3A.SH2D3A expression was significantly elevated in cervical cancer tissues. SH2D3A silencing inhibited cell proliferation and invasion, induced apoptosis, and reduced tumorigenesis in nude mice. Bioinformatics tools identified a binding relationship between SH2D3A and miR-143-3p, confirmed by the luciferase reporter assays. Western blot analysis revealed that SH2D3A knockdown led to decreased levels of Janus kinase 1 (JAK1) and signal transducer and activator of transcription 3 (STAT3) proteins. Additionally, qRT-PCR showed that SH2D3A mRNA levels decreased after HPV E7 silencing, whereas miR-143-3p levels significantly increased.HPV E7 influences SH2D3A expression through miR-143-3p, thereby regulating the JAK1/STAT3 pathway. This mechanism promotes the occurrence and development of cervical cancer.© 2025. Asian Society of Gynecologic Oncology, Korean Society of Gynecologic Oncology, and Japan Society of Gynecologic Oncology.