High expression of mitofusin-2 (MFN2), a mitochondrial fusion protein, has been frequently associated with poor prognosis of patients with cervical cancer. Here, we aimed to identify the function of MFN2 in cervical cancer to understand its influence on disease prognosis. To this end, from cervical adenocarcinoma, we performed an MTT assay and quantitative RT-PCR (qRT-PCR) analysis to assess the effects of MFN2 on the proliferation and of HeLa cells. Then, colony-formation ability and tumorigenesis were evaluated using a tumor xenograft mouse model. The migration ability related to MFN2 was also measured using a wound healing assay. Consequently, epithelial-mesenchymal transition (EMT) of MFN2-knockdowned HeLa cells originating from adenocarcinoma. markers related to MFN2 were assessed by qRT-PCR. Clinical data were analyzed using cBioPortal and The Cancer Genome Atlas. We found that MFN2 knockdown reduced the proliferation, colony formation ability, migration, and in vivo tumorigenesis of HeLa cells. Primarily, migration of MFN2-knockdowned HeLa cells decreased through the suppression of EMT. Thus, we concluded that MFN2 facilitates cancer progression and in vivo tumorigenesis in HeLa cells. These findings suggest that MFN2 could be a novel target to regulate the EMT program and tumorigenic potential in HeLa cells and might serve as a therapeutic target for cervical cancer. Taken together, this study is expected to contribute to the treatment of patients with cervical cancer.

中文翻译：

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Mitofusin-2 促进上皮间质转化诱导的宫颈癌进展。

线粒体融合蛋白mitofusin-2（MFN2）的高表达经常与宫颈癌患者的不良预后相关。在这里，我们旨在确定 MFN2 在宫颈癌中的功能，以了解其对疾病预后的影响。为此，我们从宫颈腺癌中进行了 MTT 测定和定量 RT-PCR (qRT-PCR) 分析，以评估 MFN2 对 HeLa 细胞增殖和增殖的影响。然后，使用肿瘤异种移植小鼠模型评估集落形成能力和肿瘤发生。还使用伤口愈合试验测量了与 MFN2 相关的迁移能力。因此，来自腺癌的 MFN2 敲低的 HeLa 细胞的上皮间质转化 (EMT)。通过 qRT-PCR 评估与 MFN2 相关的标记。使用 cBioPortal 和癌症基因组图谱分析临床数据。我们发现 MFN2 敲低降低了增殖、集落形成能力、迁移和HeLa 细胞的体内肿瘤发生。主要是通过抑制 EMT 减少了 MFN2 敲低的 HeLa 细胞的迁移。因此，我们得出结论，MFN2 促进HeLa 细胞中的癌症进展和体内肿瘤发生。这些发现表明 MFN2 可能是调节 HeLa 细胞 EMT 程序和致瘤潜力的新靶点，并可能作为宫颈癌的治疗靶点。综合来看，这项研究有望为宫颈癌患者的治疗做出贡献。