Cervical cancer is one of the leading female malignancy tumors worldwide. Structural maintenance of chromosomes 4 (SMC4), a member of the SMC family, is associated with cancer pathogenesis and progression. However, the role of SMC4 in cervical cancer is still unclear. In the study, SMC4 was increased in cervical cancer tissues compared with adjacent normal tissues. The SMC4 knockdown and overexpression were performed in cervical cancer cells. SMC4 knockdown inhibited cell proliferation, colony formation, cell migration and invasion, and suppressed epithelial-mesenchymal transition (EMT). Conversely, SMC4 overexpression exerted opposite effects. Moreover, SMC4 knockdown down-regulated stem cell markers, reduced the capacity of spheroid formation and inactivated NF-κB pathway. SMC4 overexpression contributed to stem cell markers, and stimulated spheroid formation and NF-κB pathway activation. Additionally, BAY11-7082 (an NF-κB inhibitor) alleviated the SMC4-mediated the effects in cervical cancer cells. In conclusion, these findings demonstrated that SMC4 overexpression facilitated the development of cervical cancer cells by activating NF-κBpathway, which provides a new therapeutic target for patients with cervical cancer.

宫颈癌是全球主要的女性恶性肿瘤之一。SMC 家族成员 4 号染色体 (SMC4) 的结构维持与癌症发病机制和进展有关。然而，SMC4在宫颈癌中的作用仍不清楚。在这项研究中，与邻近的正常组织相比，宫颈癌组织中的 SMC4 增加。SMC4 敲低和过表达在宫颈癌细胞中进行。SMC4 敲低可抑制细胞增殖、集落形成、细胞迁移和侵袭，并抑制上皮-间质转化 (EMT)。相反，SMC4 过表达产生相反的效果。此外，SMC4 敲低下调干细胞标志物，降低球体形成能力和灭活 NF-κB 通路。SMC4 过表达有助于干细胞标志物，并刺激球体形成和 NF-κB 通路激活。此外，BAY11-7082（一种 NF-κB 抑制剂）减轻了 SMC4 介导的对宫颈癌细胞的影响。总之，这些发现表明，SMC4过表达通过激活NF-κB通路促进了宫颈癌细胞的发展，为宫颈癌患者提供了新的治疗靶点。