Overexpression of SMC4 predicts a poor prognosis in cervical cancer and facilitates cancer cell malignancy phenotype by activating NF-κB pathway

• DOI: 10.1007/s13577-021-00603-2
• Publication Date: 2021-09-04T00:18:04Z
• Authors: Hui He; Cui Zheng; Yunxian Tang
• Keywords: Adenosine Triphosphatases; 0301 basic medicine; Chromosomal Proteins, Non-Histone; NF-kappa B; Gene Expression; Uterine Cervical Neoplasms; Prognosis; 3. Good health; Gene Expression Regulation, Neoplastic; 03 medical and health sciences; Phenotype; Cell Movement; Nitriles; Disease Progression; Humans; Female; Neoplasm Invasiveness; Molecular Targeted Therapy; Sulfones; Cell Proliferation; HeLa Cells; Signal Transduction

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.