Downregulation of RNF128 Inhibits the Proliferation, Migration, Invasion and EMT of Colorectal Cancer Cells

Colorectal cancer has the third highest incidence and second highest mortality rate among all cancer types. Exploring the molecular mechanisms driving malignant proliferation and metastasis of colorectal cancer will benefit the treatment and management of cancer patients. Recent studies have reported diametrically opposed roles of Ring finger protein 128 (RNF128) in different types of cancer. However, the role of RNF128 in colorectal cancer is still completely unknown, which this study attempts to analyze. The differential expression of RNF128 mRNA and protein in 30 pairs of colorectal cancer and corresponding peritumoral tissues was detected using RT-qPCR, western blot and immunohistochemical staining. siRNA specifically targeting RNF128 was transfected into colorectal cancer cell lines (SW1116 and SW480) cultured in vitro. Proliferation, growth, migration, invasion and epithelial-mesenchymal transition (EMT) of colorectal cancer cells were examined by CCK-8, clone formation, wound-healing, transwell, western blot and immunofluorescence assays. Both RNF128 mRNA and protein levels were significantly increased in colorectal cancer tissues compared to pericarcinoma tissues. Knockdown of RNF128 significantly inhibited the proliferation, growth, migration, invasion and EMT of SW480 and SW1116 cells. Targeting RNF128 may benefit the treatment and management of colorectal cancer.