Liquid crystal-based order electrically controlled q-plate system.

This paper proposes a liquid crystal-based order adjustable q-plate system. The system, which is solid-state and electrically controlled without any mechanical components, consists of several bit cells and one symbol cell. The bit cells can be electrically selected whether to modulate the beam. The magnitude of the order of the q-plate system can be controlled by activating specific bit cells. And the sign of the order can be changed by controlling the voltages in the symbol cell. The whole system can realize the function of the order adjustable q-plate with the order ranging from -2n + 1 to 2n-1 with n bit cells. In our experiment, the system with 4 bits is verified. Based on the q-plate system, the vector beams and optical vortexes with the orders ranging from -15 to 15 can be generated.

Generation of terahertz vortex pulses without any need of manipulation in the terahertz region.

Converting a Gaussian mode to a vortex beam is much more inconvenient in the terahertz (THz) region than in the near-infrared (NIR) region due to underdevelopment of THz components and strong THz diffraction. This Letter reports the direct generation of THz vortex pulses by optical difference-frequency between two NIR chirped pulses with different topological charges (TCs). By designing a passive and transmissive device for a collinear NIR pulse pair with conjugated TCs, we have experimentally obtained stable THz vortex pulses with a TC value of 2 or -2. The process needs no THz components and so is flexible to be realized and has promising applications in the THz field.

Effects of HMGA2 on the biological characteristics and stemness acquisition of gastric cancer cells.

BACKGROUND AND STUDY AIMS: The high mobility group A2 (HMGA2), a nonhistone nuclear binding protein, modulates transcription by altering the chromatin architecture of the target gene DNA in its specific AT-hooks region. HMGA2 overexpression has been observed in embryonic tissue and many malignant neoplasms. This study sought to verify whether HMGA2 plays a role in the biological functions of gastric cancer cells, such as cell proliferation, invasiveness, migration, and stem cell acquisition, and to provide some ideas for further research on the metastatic mechanism of gastric cancer. PATIENTS AND METHODS: HMGA2's effects on the proliferation, invasiveness, and migration capabilities of gastric cancer cells were individually detected by BrdU, Transwell, and wound healing assays. Western blotting and immunofluorescence were used to evaluate whether HMGA2 could promote the acquisition of gastric cancer cells. Biostatistical analyses were performed using SPSS 17.0 for Windows. RESULTS: HMGA2 expression levels in gastric cancer cell lines were significantly higher than those in human immortalized gastric epithelial cell lines (p < 0.01). Gastric cancer cell proliferation was inhibited when HMGA2 was overexpressed (p < 0.05). The invasiveness and migration capabilities of gastric cancer cells with HMGA2 overexpression were enhanced more than those of the corresponding control groups (p < 0.05). HMGA2 overexpression promotes the stemness acquisition of stem cells from gastric cancer cells. CONCLUSIONS: This study verified that the HMGA2 structural transcription factor promotes invasiveness, migration, and acquisition of gastric cancer cells. Furthermore, our findings provide significant insight for further research on the metastatic mechanism of gastric cancer.

HMGA2 elicits EMT by activating the Wnt/ß-catenin pathway in gastric cancer.

BACKGROUND: The high mobility group protein A2 (HMGA2) is an architectural transcription factor that plays an important role in the development and progression of many malignant neoplasms. High expression of HMGA2 in gastric cancer correlates with invasiveness of cancer and is an independent prognostic factor. The reason for this might be HMGA2 promoting epithelial-mesenchymal transitions (EMT), which is the key process of metastasis for some underlying mechanisms. AIMS: This study was designed to test whether HMGA2 participates in the EMT and to further understand the underlying mechanisms of EMT promoted by HMGA2. METHODS: We examined the cell biology and molecular biology changes after overexpression and knockdown HMGA2 of gastric cancer cells in vitro and vivo. To further understand the underlying mechanisms of EMT promoted by HMGA2, based on our previous study, we examined the changes of target genes of HMGA2 after overexpression and knockdown HMGA2 of gastric cancer cells. RESULTS: The results indicated that overexpressing HMGA2 enabled enhancing the oncogenic properties of gastric epithelial origin cell in vitro and in vivo. Furthermore, our study showed that HMGA2 was able to elicit EMT and regulate several genes which are closely related to the Wnt/ß-catenin pathway by directly binding to their promoter thereby activating the Wnt/ß-catenin pathway. CONCLUSIONS: The Wnt/ß-catenin pathway activated by HMGA2 might be the underlying mechanism of EMT in gastric cancer cells.

Clinicopathological significance of platelet-derived growth factor B, platelet-derived growth factor receptor-ß, and E-cadherin expression in gastric carcinoma.

AIM OF THE STUDY: Platelet-derived growth factor B (PDGF-B), a vital growth factor which can induce angiogenesis and epithelial-mesenchymal transition (EMT), is important in the metastasis of many tumors. However, the roles of PDGF-B in gastric carcinoma are largely unknown. We investigated the correlation between PDGF-B, PDGFR-ß and E-cadherin expression with the clinical features of gastric carcinoma patients to evaluate the relationship between PDGF-B signaling, E-cadherin and metastasis of gastric carcinoma, the correlation between PDGF-B and E-cadherin expression to assess the roles of PDGF-B signaling in metastasis of gastric carcinoma.. MATERIAL AND METHODS: We detected expressions of PDGF-B, PDGFR-ß and E-cadherin in gastric carcinoma tissues and normal gastric mucosa tissues of 64 patients with gastric carcinoma who had undergone surgical resection, and investigated their relationships with clinical features and the relationships between PDGF-B and E-cadherin expression in gastric carcinoma. RESULTS: In surgical specimens, tumor cells expressed PDGF-B, and PDGFR-ß was expressed by tumor stromal cells. E-cadherin was expressed by both tumor cells and normal gastric mucosa cells. Expressions of PDGF-B and PDGFR-ß were increased in gastric carcinoma tissues (p < 0.05) and were positively correlated with the depth of cancer invasion, lymph node metastasis and TNM stage (p < 0.05). The expression of E-cadherin was reduced in gastric carcinoma tissues (p < 0.05) and was negatively correlated with the depth of cancer invasion, lymph node metastasis and TNM stage (p < 0.05). The correlation between PDGF-B and E-cadherin expression was negative (p < 0.05). CONCLUSION: Our data indicate that either the overexpression of PDGF-B and PDGFR-ß or the underexpression of E-cadherin is correlated with cancer progression and lymphogenous metastasis of gastric carcinoma. The PDGF-B signal pathway might induce EMT by down-regulating expression of E-cadherin to promote metastasis of gastric carcinoma.

DNA methylation-related lncRNAs predict prognosis and immunotherapy response in gastric cancer.

BACKGROUND: LncRNAs and DNA methylation are both key regulators of tumorigenesis and immune regulation. However, the interaction between lncRNA and DNA methylation, their regulation and their clinical and immune relevance in gastric cancer (GC) remain unclear. METHODS: In this study, we identified DNA methylation regulator-related lncRNAs through Pearson correlation analysis in The Cancer Genome Atlas datasets. Univariate Cox regression was used to screen DNA methylationrelated prognostic lncRNAs. Further, through least absolute shrinkage and selection operator Cox regression, a prognostic model based on 13 lncRNAs was established. Survival analysis and receiver operating characteristic curve analysis verified the accuracy of the model in predicting the survival of GC patients. Univariate and multivariate analyses also confirmed that the risk score obtained from the risk model could be applied as an independent prognostic factor for patients with GC. Furthermore, based on the risk score and other clinicopathological characteristics that can be used as independent prognostic factors, we constructed a nomogram that could accurately determine the survival time of each patient. In addition, a lncRNA score was constructed using a principal component analysis algorithm to quantify the DNA methylation-related lncRNA expression patterns of individual tumors. RESULTS: We found that a higher lncRNA score indicated a worse the prognosis and was associated with a reduced tumor mutation burden and immunosuppression. A low lncRNA score was related to an increase in neoantigen load and an increase in the anti-PDL1/CTLA4 immunotherapy response. Additionally, a low lncRNA score was related to a significant therapeutic advantage and clinical benefit. CONCLUSIONS: This study describes a DNA methylation regulator-related lncRNA signature model, which provides a new approach for predicting therapeutic response and patient stratification in GC. Assessing lncRNA expression patterns in individual tumors will contribute to enhancing our understanding of tumor microenvironment infiltration and guide more effective immunotherapy strategies.

Transcriptomic analysis reveals the promotion of lymph node metastasis by Helicobacter pylori infection via upregulating chemokine (C-X-C motif) receptor 2 expression in gastric carcinoma.

Gastric carcinoma (GC) progression is mainly caused by local aggression and lymph node metastasis. However, some patients with early T-stage disease have lymph node metastasis, whereas some patients with late T-stage disease do not have lymph node metastasis, which indicates that invasion and metastasis are not always sequential in some GC patients. In the present study, the data of 101 GC cases were acquired from TCGA and divided into T-late-N-negative and T-early-N-positive groups according to pathological stages. A total of 338 genes were identified as differential genes between the T-late-N-negative and T-early-N-positive groups. GSEA showed that epithelial cell signaling in the Helicobacter pylori (HP) infection pathway was enriched in the T-early-N-positive group. MB staining indicated that the HP infection rate was 63% (39/62) in N-positive patients compared to 42% (16/38) in N-negative patients. To investigate the potential mechanism, we focused on the gene chemokine (C-X-C motif) receptor 2 (CXCR2), which was not only clustered in the gene set of epithelial cells signaling in the HP infection pathway but also significantly upregulated in T-early-N-positive GC by the analysis of the different genes based on the TCGA dataset. A meta-analysis showed that CXCR2 expression was positively correlated with N-stage but not with T-stage in GC. This study indicated that invasion and metastasis could be independent processes driven by different molecular mechanisms in some GC patients. HP infection was a potential factor that promoted lymph node metastasis by upregulating CXCR2 expression.

Genome-wide analysis of HMGA2 transcription factor binding sites by ChIP on chip in gastric carcinoma cells.

High mobility group protein A2 (HMGA2) is an architectural transcription factor that plays an important role in development and progression of malignant neoplasias. Recently, some studies reported that HMGA2 is also implicated in epithelial-mesenchymal transitions (EMT) and cancer stem cells. But the underlying mechanisms of these conditions are poorly understood. Therefore, we established an EMT model of gastric carcinoma cells by overexpressing HMGA2 in vitro, then global mapping of HMGA2 potential transcription factor binding sites was identified by promoter microarray in these cells, and the date obtained from the microarrays were validated via chromatin immunoprecipitation-PCR (ChIP-PCR) and real-time PCR. HMGA2 potential target genes were classified in KEGG database and Gene Ontology (GO) analyses. To our knowledge, this is the first report on the genome-wide analysis of HMGA2 downstream direct targets, and these findings will be valuable in understanding the roles of HMGA2 in EMT.

High level of WAVE1 expression is associated with tumor aggressiveness and unfavorable prognosis of epithelial ovarian cancer.

OBJECTIVES: Wiskott-Aldrich syndrome protein family verprolin-homologous protein 1 (WAVE1) has been shown to promote cancer invasion and metastasis. However, no evidence has been found to identify the role of WAVE1 in epithelial ovarian cancer (EOC). This study aims to determine the effect of WAVE1 expression and investigate a possible relationship between WAVE1 and prognosis in EOC. METHODS: WAVE1 protein level was measured in 223 EOC specimens by immunohistochemical staining and 46 EOC specimens by Western blot analysis. Expression of WAVE1 in ovarian cancer cell lines was evaluated by Western blot analysis and immunofluorescence. Survival analysis was performed to assess the correlation between WAVE1 expression and survival. RESULTS: Immunohistochemical staining and Western blot analysis showed that WAVE1 was overexpressed in EOC compared with samples from a non-invasive ovarian tumor and normal ovaries (P<0.05). Furthermore, expression of WAVE1 was significantly associated with advanced FIGO stage, poor grade, serum Ca-125 and residual tumor size (P<0.05). By Western blot analysis, WAVE1 expression was detected in four ovarian cancer cell lines. Immunofluorescence was performed to demonstrate WAVE1 expression in SKOV3 and 3AO cell lines. Survival analysis showed that patients with low WAVE1 staining had a significantly better survival compared to patients with high WAVE1 staining (P<0.05). In multivariate analysis, WAVE1 overexpression, advanced stage and suboptimal surgical debulking were independent prognostic factors of poor survival. CONCLUSIONS: Our present study finds that WAVE1 overexpression is associated with an unfavorable prognosis. WAVE1 is an independent prognostic factor for EOC, which suggests that it is a novel and crucial predictor for EOC metastasis.

Construction and Comprehensive Prognostic Analysis of a Novel Immune-Related lncRNA Signature and Immune Landscape in Gastric Cancer.

Gastric cancer (GC) is a malignant tumor with high mortality and poor prognosis. Immunotherapies, especially immune checkpoint inhibitors (ICI), are widely used in various tumors, but patients with GC do not benefit much from immunotherapies. Therefore, effective predictive biomarkers are urgently needed for GC patients to realize the benefits of immunotherapy. Recent studies have indicated that long noncoding RNAs (lncRNAs) could be used as biomarkers in the immune landscape of multiple tumors. In this study, we constructed a novel immune-related lncRNA (irlncRNA) risk model to predict the survival and immune landscape of GC patients. First, we identified differentially expressed irlncRNAs (DEirlncRNAs) from RNA-Seq data of The Cancer Genome Atlas (TCGA). By using various algorithms, we constructed a risk model with 11 DEirlncRNA pairs. We then tested the accuracy of the risk model, demonstrating that the risk model has good efficiency in predicting the prognosis of GC patients. Inner validation sets were further used to confirm the effectiveness of the risk model. In addition, our risk model has a preferable performance in predicting the immune infiltration status of tumors, immune checkpoint status of the patients, and immunotherapy score. In conclusion, our risk model may provide insights into the prognosis of and immunotherapy strategy for GC.

Repetitive non-typhoidal Salmonella exposure is an environmental risk factor for colon cancer and tumor growth.

During infection, Salmonella hijacks essential host signaling pathways. These molecular manipulations disrupt cellular integrity and may induce oncogenic transformation. Systemic S. Typhi infections are linked to gallbladder cancer, whereas severe non-typhoidal Salmonella (NTS) infections are associated with colon cancer (CC). These diagnosed infections, however, represent only a small fraction of all NTS infections as many infections are mild and go unnoticed. To assess the overall impact of NTS infections, we performed a retrospective serological study on NTS exposure in patients with CC. The magnitude of exposure to NTS, as measured by serum antibody titer, is significantly positively associated with CC. Repetitively infecting mice with low NTS exposure showed similar accelerated tumor growth to that observed after high NTS exposure. At the cellular level, NTS preferably infects (pre-)transformed cells, and each infection round exponentially increases the rate of transformed cells. Thus, repetitive exposure to NTS associates with CC risk and accelerates tumor growth.

Corrigendum to "SOX4 contributions to TGF-ß-induced endothelial-mesenchymal transition and stem cell characteristics of gastric cancer cells" [Genes & Diseases 5 (2018) 49-61].

[This corrects the article DOI: 10.1016/j.gendis.2017.12.005.].

Identification and Comprehensive Prognostic Analysis of a Novel Chemokine-Related lncRNA Signature and Immune Landscape in Gastric Cancer.

Gastric cancer (GC) is a malignant tumor with poor survival outcomes. Immunotherapy can improve the prognosis of many cancers, including GC. However, in clinical practice, not all cancer patients are sensitive to immunotherapy. Therefore, it is essential to identify effective biomarkers for predicting the prognosis and immunotherapy sensitivity of GC. In recent years, chemokines have been widely reported to regulate the tumor microenvironment, especially the immune landscape. However, whether chemokine-related lncRNAs are associated with the prognosis and immune landscape of GC remains unclear. In this study, we first constructed a novel chemokine-related lncRNA risk model to predict the prognosis and immune landscape of GC patients. By using various algorithms, we identified 10 chemokine-related lncRNAs to construct the risk model. Then, we determined the prognostic efficiency and accuracy of the risk model. The effectiveness and accuracy of the risk model were further validated in the testing set and the entire set. In addition, our risk model exerted a crucial role in predicting the infiltration of immune cells, immune checkpoint genes expression, immunotherapy scores and tumor mutation burden of GC patients. In conclusion, our risk model has preferable prognostic performance and may provide crucial clues to formulate immunotherapy strategies for GC.

Salmonella Infection in Chronic Inflammation and Gastrointestinal Cancer.

Salmonella not only causes acute infections, but can also cause patients to become chronic "asymptomatic" carriers. Salmonella has been verified as a pathogenic factor that contributes to chronic inflammation and carcinogenesis. This review summarizes the acute and chronic Salmonella infection and describes the current research progress of Salmonella infection contributing to inflammatory bowel disease and cancer. Furthermore, this review explores the underlying biological mechanism of the host signaling pathways manipulated by Salmonella effector molecules. Using experimental animal models, researchers have shown that Salmonella infection is related to host biological processes, such as host cell transformation, stem cell maintenance, and changes of the gut microbiota (dysbiosis). Finally, this review discusses the current challenges and future directions in studying Salmonella infection and its association with human diseases.

Circular RNA circGRAMD1B inhibits gastric cancer progression by sponging miR-130a-3p and regulating PTEN and p21 expression.

Circular RNAs (circRNAs) have emerged as essential regulators and biomarkers of various cancers. However, the effects of a novel circRNA termed circGRAMD1B in human gastric cancer (GC) remain unclear. A microarray was used to screen circRNA expression in GC. Quantitative real-time PCR was used to detect the expression of circGRAMD1B. Gain- and loss- of-function experiments were performed to investigate the biological functions of circGRAMD1B in vitro and vivo. Bioinformatics analysis, fluorescence in situ hybridization, dual-luciferase reporter assay, RNA immunoprecipitation, RNA pull-down assay, and rescue experiments were conducted to confirm the underlying mechanisms of competitive endogenous RNAs (ceRNAs). We screened differentially expressed circRNAs and found that circGRAMD1B expression was downregulated in GC tissues and cell lines. Functionally, circGRAMD1B acted as an anti-oncogene and inhibited the proliferation, migration, and invasion abilities of GC cells. Then, we verified that circGRAMD1B served as a sponge that targeted miR-130a-3p in GC cells; circGRAMD1B alleviated GC cell proliferation, migration, and invasion by targeting miR-130a-3p. A mechanistic analysis showed that PTEN and p21 were involved in circGRAMD1B/miR-130a-3p axis-inhibited GC tumorigenesis. Our findings suggest that circGRAMD1B plays an important role in GC progression by regulating miR-130a-3p-PTEN/p21, which may provide a potential biomarker and therapeutic target for GC.

HOXA5 is a tumor suppressor gene that is decreased in gastric cancer.

The abnormal expression of homeobox A5 (HOXA5) has been observed in breast and colon cancer; however, the clinical significance of HOXA5 in gastric cancer (GC) is not yet clear. In this study, we found that HOXA5 expression was decreased in GC tissues at the mRNA and protein level compared with paracancerous tissues using reverse transcription­quantitative PCR (RT­qPCR) and western blot analysis, respectively. Immunohistochemistry and Kaplan­Meier survival analysis confirmed that the underexpression of HOXA5 was associated with GC progression and indicated a poor prognosis of patients with GC. Given that proliferation­related genes may be potential target genes of HOXA5, we performed a series of experiments in vitro to examine the effects of HOXA5 on the proliferation of GC cells. A CCK­8 assay, colony formation assay and flow cytometry revealed that HOXA5 inhibited the abnormal proliferation of GC cells, and this finding was further supported by a 5­ethynyl­2'­deoxyuridine (EdU) assay. Further mechanistic investigation clarified that HOXA5 promoted the protein expression of p21 and inhibited the protein expression of c­Myc and Ki67. Additionally, the use of nude mouse models also verified that HOXA5 suppressed the proliferation of GC cells in vivo. Collectively, the findings of this study demonstrate that HOXA5 acts as a tumor suppressor gene during the development and progresion of GC, possibly functioning by inhibiting the abnormal proliferation of cancer cells.

SOX4 contributes to TGF-ß-induced epithelial-mesenchymal transition and stem cell characteristics of gastric cancer cells.

SOX4 is highly expressed in gastric cancer (GC) and is associated with tumor grade, metastasis and prognosis, however the mechanism is not clear. We report herein that SOX4 was upregulated and overexpression of SOX4 was associated with increased expression of the markers of Epithelial-mesenchymal transition (EMT) and stemness in clinic patient samples. In vitro, overexpression of SOX4 promoted the invasion as showed by Transwell assay and stemness of GC cells as assessed by sphere formation assay, which was suppressed by silencing SOX4 with shRNA. Further studies showed that SOX4 up-regulated the expression of EMT transcription factors Twist1, snail1 and zeb1 and stemness transcription factors SOX2 and OCT4, and promoted the nuclear translocation of ß-catenin. Moreover, we revealed that TGF-ß treatment significantly up-regulated the expression of SOX4 and silencing SOX4 reversed TGF-ß induced invasion and sphere formation ability of GC cells. Finally, we showed that SOX4 promoted the lung metastasis and tumor formation ability of gastric cancer cells in nude mice. Our results suggest that SOX4 is a target TGF-ß signaling and mediates TGF-ß-induced EMT and stem cell characteristics of GC cells, revealing a novel role of TGF-ß/SOX4 axis in the regulation of malignant behavior of GC.

DIMT1 overexpression correlates with progression and prognosis in gastric carcinoma.

We investigated the expression of dimethyladenosine transferase 1 homolog (DIMT1) in human gastric carcinoma (GC) tissues, pericarcinoma histologically normal tissues, and normal gastric tissues and explored its clinical significance. Immunohistochemistry staining was used to detect the expression of DIMT1, and the findings were compared with clinicopathological features of patients with GC. The result also was ascertained by Western blotting. The Kaplan-Meier method and log-rank test were used to compare the overall survival rate and time in the DIMT1 low-level and high-level expression groups. Immunohistochemical staining indicated that the expression of DIMT1 in GC tissues (65/75; 86.7%) was significantly more common (P<.001) than that in pericarcinoma histologically normal tissues (14/75; 18.7%) and normal gastric tissues (2/12; 16.7%). High expression of DIMT1 correlated closely with differentiation (P=.023), invasion (P=.042), lymph node metastasis (P=.008), distant metastasis (P=.006), and TNM stage (P=.013). Western blotting showed that DIMT1 expression correlated positively with TNM stage and implied that more advanced TNM stage was accompanied by higher expression of DIMT1 (P<.001). Kaplan-Meier survival analysis showed that high DIMT1 expression correlated significantly (P<.001) with a poor prognosis. Our data suggest that DIMT1 is a useful molecular biomarker to predict tumor progression and prognosis in patients with GC.

HMGA2 regulates epithelial-mesenchymal transition and the acquisition of tumor stem cell properties through TWIST1 in gastric cancer.

High expression of high mobility group protein A2 (HMGA2) is correlated with the invasiveness of gastric cancer and is an independent prognostic factor. The reason may be that HMGA2 promotes epithelial-mesenchymal transition (EMT) and the acquisition of tumor stem cell properties, yet the mechanism remains unclear. In this study, immunohistochemistry and western blot analysis revealed that the expression of HMGA2 and Twist-related protein 1 (TWIST1) in gastric carcinoma tissues was higher than that in the peritumoral tissues and that the expression levels of these two proteins were positively correlated. The protein expression levels of HMGA2 and TWIST1 were high in the poorly differentiated gastric cancer MKN-45 cells and were low in the moderately differentiated SGC-7901 cells. TWIST1 was inhibited after HMGA2 interference and was significantly increased after overexpression of HMGA2. Luciferase experiments showed that TWIST1 was a direct downstream target gene of HMGA2. The simultaneous interference of HMGA2 expression and the overexpression of TWIST1 in MKN-45 cells reversed the inhibitory effect of HMGA2 interference on the invasion and migration of gastric cancer cells, EMT and the expression of stemness markers. However, the simultaneous overexpression of HMGA2 and the interference of TWIST1 expression in the SGC-7901 cells reversed the promoter effect of HMGA2 overexpression on the invasiveness and migration of gastric cancer cells, EMT and the expression of stemness markers. In addition, animal experiments showed that TWIST1 overexpression reversed the inhibition of HMGA2 interference on the metastasis of MKN-45 cells. Therefore, HMGA2 regulates the EMT of gastric cancer cells and the acquisition of tumor stem cell properties through direct regulation of the downstream target gene TWIST1.

Upregulation of GNL3 expression promotes colon cancer cell proliferation, migration, invasion and epithelial-mesenchymal transition via the Wnt/ß-catenin signaling pathway.

G protein nucleolar 3 (GNL3), a nucleolar GTP-binding protein, is highly expressed in progenitor cells, stem cells, and various types of cancer cells. Therefore, it is considered to have an important role in cancer pathogenesis. GNL3 has been reported to play crucial roles in cell proliferation, cell cycle regulation, inhibition of differentiation, ribosome biogenesis, and the maintenance of stemness, genome stability and telomere integrity. Furthermore, GNL3 has recently been shown to be involved in cancer invasion and metastasis. However, the biological significance of GNL3 in the invasion and metastasis of colon cancer remains unclear. This study was performed to address this gap in knowledge. GNL3 expression was upregulated in colon cancer tissue specimens and correlated with tumor differentiation, invasion and metastasis. GNL3 overexpression promoted cell proliferation, invasion, migration and the epithelial-mesenchymal transition (EMT) in colon cancer cells. Moreover, inhibition of the EMT and the Wnt/ß­catenin signaling pathway induced by GNL3 knockdown was partially reversed by lithium chloride (LiCl). Based on these data, GNL3 promotes the EMT in colon cancer by activating the Wnt/ß­catenin signaling pathway. In summary, GNL3 is upregulated in colon cancer and plays an important role in tumor growth, invasion and metastasis. Strategies targeting GNL3 are potential treatments for colon cancer.