SMC1 promotes proliferation and inhibits apoptosis through the NF‑κB signaling pathway in colorectal cancer
- Jin Li
- Jingdong He
- Yuan Wang
- Yongqian Shu
- Jianwei Zhou
Affiliations: Department of Oncology, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China, Department of Oncology, The Affiliated Huai'an No. 1 People's Hospital of Nanjing Medical University, Huai'an, Jiangsu 223300, P.R. China, Department of Oncology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu 210029, P.R. China, Department of Molecular Cell Biology and Toxicology, Center of Global Health, School of Public Health, Nanjing Medical University, Nanjing, Jiangsu 211166, P.R. China
- Published online on: August 8, 2019 https://doi.org/10.3892/or.2019.7273
Copyright: © Li
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Colorectal cancer (CRC) is the third most common cancer and a leading cause of cancer‑associated mortality globally. Increasing evidence has indicated that structural maintenance of chromosomes 1 (SMC1) may serve an important role in solid tumors as a tumor enhancer. In the present study, it was identified via reverse transcription‑quantitative PCR and western blot analyses that expression of SMC1 was significantly upregulated in CRC cell lines (SW480, HCT‑116 and SW620) compared with NCM460 normal epithelial cells. To determine the potential involvement of SMC1 in the malignant phenotypes of CRC cells, SMC1 was knocked down in SW620 cells and SMC1 was overexpressed in SW480 cells in vitro. As a result, cell viability, proliferation, invasion and migration were suppressed in transduced SW620 cells but enhanced in SW480 cells, as determined using MTT, colony formation and Transwell assays; conversely, flow cytometric analysis revealed that cell apoptosis was increased in SW620 cells and inhibited in SW480 cells following lentiviral infection. In addition, an in vivo mouse xenograft model revealed that knocking down SMC1 suppressed tumor growth and increased apoptosis; however, overexpressing SMC1 enhanced tumor growth and suppressed apoptosis. Further experiments demonstrated that the role of SMC1 on CRC may involve downregulation of the NF‑κB‑associated signaling pathway. Finally, the present data from clinical CRC tumor samples showed that increased expression of SMC1 was significantly associated with distant metastasis, higher TNM stage, primary tumor size, lymph node metastasis and worse overall survival. Collectively, the present results suggested that SMC1 served an important role in the development of CRC and may be a predictive prognostic biomarker in patients with CRC.