Original Article
Effect of NOP2 knockdown on colon cancer cell proliferation, migration, and invasion
Abstract
Background: Proliferation-associated nucleolar protein p120 (NOP2) has been proven to be a promising tumor cell maker, but it has not been specifically studied in colon cancer. This study aims to investigate the role and action mechanism of NOP2 in colon cancer.
Methods: Fluorescence quantitative PCR and western blot assays were used to evaluate the expression of NOP2. NOP2 siRNA was transfected into HCT116, LOVO, and CCK-8 cells, and transwell assays were performed to evaluate the cell proliferation, migration, and invasion. Transcriptome sequencing of both the NOP2 knockdown and negative control (NC) groups was performed.
Results: NOP2 expression is significantly upregulated in colon cancer tissues and cells compared with that in the healthy controls. The proliferation, migration, and invasion of the colon cancer cells were significantly suppressed in the NOP2 knockdown group compared with those in the NC group (P<0.05). Transcriptome sequencing showed that ASMTL and C6orf52 were significantly downregulated, while MUC19, TXK, APOBEC2, and RBM44 were upregulated in both of the two NOP2 silenced colon cancer cells relative to those in the control. Gene Ontology (GO) analysis showed that NOP2 knockdown mainly induced differential expression of the genes involved in positive regulation of T cell-mediated cytotoxicity and thiamine metabolism. Kyoto Encyclopedia of Genes and Genomes analysis showed that the gene pathways most significantly affected by NOP2 knockdown were Cytokine-cytokine receptor interaction, Type I diabetes mellitus, Taste transduction, and Systemic lupus erythematosus.
Conclusions: NOP2 promotes proliferation, migration, and invasion of colon cancer cells, and the underlying mechanisms may be related to TXK tyrosine kinase.
Methods: Fluorescence quantitative PCR and western blot assays were used to evaluate the expression of NOP2. NOP2 siRNA was transfected into HCT116, LOVO, and CCK-8 cells, and transwell assays were performed to evaluate the cell proliferation, migration, and invasion. Transcriptome sequencing of both the NOP2 knockdown and negative control (NC) groups was performed.
Results: NOP2 expression is significantly upregulated in colon cancer tissues and cells compared with that in the healthy controls. The proliferation, migration, and invasion of the colon cancer cells were significantly suppressed in the NOP2 knockdown group compared with those in the NC group (P<0.05). Transcriptome sequencing showed that ASMTL and C6orf52 were significantly downregulated, while MUC19, TXK, APOBEC2, and RBM44 were upregulated in both of the two NOP2 silenced colon cancer cells relative to those in the control. Gene Ontology (GO) analysis showed that NOP2 knockdown mainly induced differential expression of the genes involved in positive regulation of T cell-mediated cytotoxicity and thiamine metabolism. Kyoto Encyclopedia of Genes and Genomes analysis showed that the gene pathways most significantly affected by NOP2 knockdown were Cytokine-cytokine receptor interaction, Type I diabetes mellitus, Taste transduction, and Systemic lupus erythematosus.
Conclusions: NOP2 promotes proliferation, migration, and invasion of colon cancer cells, and the underlying mechanisms may be related to TXK tyrosine kinase.
