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.

Differential Regulation of Genes by the Glucogenic Hormone Asprosin in Ovarian Cancer

“…Genes that were commonly expressed at both 4 and 12 h were chosen for analysis, in addition to their association with cancer in the literature [ 33 , 34 , 35 ]. FCGR2A, MAGI2-AS3 and TXK were up-regulated on initial treatment with asprosin and show a similar increase in expression upon repeat and validation with RT-qPCR, albeit to a lesser effect than seen in RNA sequencing ( Figure 6 ).…”

Human NOP2/NSUN1 Regulates Ribosome Biogenesis Through Non-Catalytic Complex Formation with Box C/D snoRNPs

“…In line with an essential role for NOP2/NSUN1, our attempts to generate CRISPR knockouts were not successful and the only clones that could be recovered were NOP2/NSUN1 mutant heterozygotes alleles or homozygous mutants with destabilized mRNA leading to low levels of NOP2/NSUN1 protein production (not shown). NOP2/NSUN1 is overexpressed in a wide variety of cancer, and its expression level correlates with tumor aggressiveness, poor prognosis and therapy resistance (22,23,(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)107). NOP2/NSUN1 depletion has been shown to suppress proliferation, migration, and invasion of colon cancer cells (107) and sensitize leukemia cells to 5-aza-cytidine treatment (108).…”

“…NOP2/NSUN1 is overexpressed in a wide variety of cancer, and its expression level correlates with tumor aggressiveness, poor prognosis and therapy resistance (22,23,(25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35)107). NOP2/NSUN1 depletion has been shown to suppress proliferation, migration, and invasion of colon cancer cells (107) and sensitize leukemia cells to 5-aza-cytidine treatment (108). Although inhibition of ribosome biogenesis is known to induce cell cycle arrest through p53 activation (75)(76)(77)(78)(79)(80)(81)(82)(83)(84)(85)(86)(87)(88), our data demonstrate that depletion of NOP2/NSUN1 severely impairs cell proliferation in both WT and p53-null cells.…”

Mammalian Neuraminidases in Immune-Mediated Diseases: Mucins and Beyond

“…Transcriptome analysis of nucleolar protein p120 (NOP2)-deficient vs . NOP2-expressing human colon cancer cells identified the MUC19 gene as significantly upregulated, and T1D as a gene pathway most significantly affected, by NOP2 silencing ( 367 ). Future studies are needed to determine whether NEUs regulate MUC-associated diabetes.…”