CDC23 knockdown suppresses the proliferation, migration and invasion of liver cancer via the EMT process

• Published in: Oncology letters Vol. 26; no. 1; p. 1
• Main Authors: Zhang, Yang, Luo, Lianghua, Fu, Chengchao, Hu, Wang, Li, Yong, Xiong, Jianbo
• Format: Journal Article
• Language: English
• Published: Athens Spandidos Publications 01-07-2023; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Antibodies; Cancer; Cell cycle; Cell division; Cell growth; Ethylenediaminetetraacetic acid; Experiments; Genetic aspects; Health aspects; Liver cancer; Membranes; Mortality; Oncology; Protein expression; Proteins; Scientific equipment and supplies industry; Thyroid cancer; United States; China
• ISSN: 1792-1074; 1792-1082
• DOI: 10.3892/ol.2023.13877

Liver cancer (LC) is a malignant tumour that is associated with high mortality rates worldwide. Cell division cycle 23 (CDC23) acts as an oncogene in papillary thyroid cancer. In addition, epithelial-mesenchymal transition (EMT) is frequently involved in the malignant metastasis of various cancer types. Therefore, we hypothesized that CDC23 may regulate the malignant biological behaviours of LC cells through EMT. Proliferation, colony formation and Transwell assays, western blotting and xenograft experiments were performed. The results of the present study showed that CDC23 was highly expressed in LC cell lines. In addition, it was found via multiple in vitro assays that CDC23 knockdown reduced the proliferation, migration and invasion of LC cell lines. Finally, an in vivo study confirmed that CDC23 knock-down inhibited the growth of xenograft LC in nude mice. More importantly, the changes in the levels of EMT-related marker proteins were analysed in the sh-CDC23 group compared with the sh-NC group of cells and xenografts. E-cadherin was upregulated, and N-cadherin and vimentin were significantly downregulated after CDC23 silencing. Taken together, these results revealed that the knockdown of CDC23 inhibits the progression of LC by regulating EMT and that CDC23 may be a novel therapeutic target for LC.