Cervical cancer (CC) is the second most common type of cancer in women, and presents a serious threat to public health. We aimed to investigate the regulatory impacts of CDGSH iron-sulfur domain-containing protein 2 (CISD2) in CC and to discuss its relationship with E2F transcription factor 7 (E2F7). With the employment of real-time reverse transcriptase-polymerase chain reaction (RT-qPCR) and western blot, the expression of CISD2 and E2F7 in SiHa cells before or after transfection was estimated. Cell counting kit-8 (CCK-8) assay, Terminal deoxynucleotidyl transferase (TdT) dUTP Nick-End Labeling (TUNEL) assay, wound healing and transwell were used to detect the proliferation, apoptosis, migration and invasion of SiHa cells. The activity of CISD2 was detected using luciferase report assay and chromatin immunoprecipitation (ChIP) assay was used to confirm the binding of E2F7 and CISD2 promoter. The contents of proliferation- and apoptosis-related proteins were detected using western blot. Results revealed that CISD2 expression was greatly enhanced in CC cell lines. CISD2 depletion inhibited the proliferation, migration and invasion of SiHa cells but promoted the cell apoptosis. It was also found that E2F7 was remarkably elevated in SiHa cells. According to JASPAR database, the binding sites of E2F7 and CISD2 were predicted and ChIP confirmed the binding of E2F7 and CISD2 promoter. Results obtained from luciferase report assay indicated that E2F7 overexpression increased the activity of CISD2 promoter region. Furthermore, further functional experiments demonstrated that the impacts of E2F7 interference on the proliferation, migration, invasion and apoptosis of SiHa cells were reversed by CISD2 overexpression. In summary, CISD2 silence could alleviate the malignant progression of CC and could be transcribed by E2F7.

宫颈癌（CC）是女性第二常见的癌症类型，对公共健康构成严重威胁。我们的目的是研究 CDGSH 含铁硫结构域蛋白 2 (CISD2) 在 CC 中的调控影响，并讨论其与 E2F 转录因子 7 (E2F7) 的关系。利用实时逆转录聚合酶链反应（RT-qPCR）和蛋白质印迹，估计转染前后SiHa细胞中CISD2和E2F7的表达。采用细胞计数试剂盒8（CCK-8）检测、末端脱氧核苷酸转移酶（TdT）dUTP缺口末端标记（TUNEL）检测、伤口愈合和Transwell检测SiHa细胞的增殖、凋亡、迁移和侵袭。使用荧光素酶报告测定检测CISD2的活性，并使用染色质免疫沉淀（ChIP）测定来确认E2F7和CISD2启动子的结合。采用western blot检测增殖和凋亡相关蛋白的含量。结果显示 CISD2 表达在 CC 细胞系中大大增强。CISD2缺失抑制SiHa细胞的增殖、迁移和侵袭，但促进细胞凋亡。还发现 SiHa 细胞中 E2F7 显着升高。根据JASPAR数据库预测E2F7和CISD2的结合位点，ChIP证实E2F7和CISD2启动子的结合。荧光素酶报告测定结果表明，E2F7 过表达增加了 CISD2 启动子区域的活性。此外，进一步的功能实验表明，E2F7干扰对SiHa细胞增殖、迁移、侵袭和凋亡的影响可通过CISD2过表达而逆转。综上所述，CISD2沉默可以减轻CC的恶性进展，并且可以被E2F7转录。