miR-145-5p靶向TAGLN2调控结直肠癌SW620细胞侵袭和迁移的机制探讨

目的:探究微小RNA-145-5p（miR-145-5p）在结直肠癌组织和细胞中的表达情况及其靶向调控肌动蛋白凝胶蛋白2（TAGLN2）对结直肠癌细胞侵袭和迁移能力的影响。方法:采用实时荧光定量PCR（qPCR）技术对48例结直肠癌患者癌组织、配对癌旁组织、结直肠癌细胞株（HCT8、SW620、HCT116、HT-29）及结直肠黏膜细胞FHC中的miR-145-5p和TAGLN2 mRNA表达进行定量分析。将SW620细胞设为空白对照组、miR-145-5p mimics组、mimics-NC组、pcDNA3.1-TAGLN2组、pcDNA3.1-Vector组和miR-145-5p mimics+pcDNA3.1-TAGLN2组,采用qPCR检测miR-145-5p和TAGLN2 mRNA表达,采用Transwell法检测细胞侵袭及迁移能力,采用免疫印迹法（Western blot）检测TAGLN2蛋白及EMT相关蛋白表达,采用双荧光素酶报告实验检测miR-145-5p和TAGLN2间的靶向关系。结果:miR-145-5p在结直肠癌组织中的表达水平显著低于癌旁组织（P<0.05）,并与结直肠癌患者的TNM分期和淋巴结转移相关（均P<0.05）;TAGLN2在结直肠癌组织中的表达水平显著高于癌旁组织,并与miR-145-5p表达呈负相关（P<0.05）;miR-145-5p和TAGLN2在结直肠癌HCT8、SW620、HCT116和HT-29细胞中的表达水平显著低于或高于FHC细胞（均P<0.05）。miR-145-5p过表达可降低SW620细胞的侵袭和迁移能力。miR-145-5p靶向调控TAGLN2表达,单独转染TAGLN2阳性质粒可增加SW620细胞的侵袭和迁移能力,与miR-145-5p mimics同时转染后,TAGLN2蛋白、波形蛋白（Vimentin）和神经钙黏素（N-cadherin）表达降低,上皮钙黏素（E-cadherin）表达升高,TAGLN2对SW620细胞侵袭和迁移能力的增强作用被显著抑制。结论:miR-145-5p在结直肠癌中呈低表达状态,其表达水平与结直肠癌患者的TNM分期和淋巴结转移密切相关,miR-145-5p靶向调控TAGLN2抑制结直肠癌细胞的侵袭和迁移能力。     

miR-23b-3p在结直肠癌中的表达及其靶向KLF3抑制结直肠癌细胞侵袭和迁移能力的机制研究

目的:研究miR-23b-3p在结直肠癌中的表达情况及对结直肠癌SW620细胞侵袭和迁移的影响机制。方法:收集2018年01月至2020年12月我院胃肠外科手术切除的58例结直肠癌组织及癌旁组织标本,以及结直肠癌细胞株SW480、SW620、HCT116、HT-29、Lovo和人正常结直肠黏膜细胞FHC,采用qPCR法检测miR-23b-3p和KLF3相对表达水平。采用脂质体转染技术将miR-23b-3p mimics、mimics-NC转染至SW620细胞,采用Transwell实验和划痕实验检测其侵袭和迁移能力的改变。利用生物信息学软件预测并通过双荧光素酶报告基因实验验证miR-23b-3p和KLF3的结合位点。将KLF3过表达质粒（pcDNA3.1-KLF3）或空载质粒（Vector）单独或联合miR-23b-3p mimics转染至SW620细胞,采用Transwell实验和划痕实验检测其侵袭和迁移能力的改变,采用qPCR和Western Blot实验检测SW620细胞中KLF3 mRNA及蛋白的表达。结果:miR-23b-3p在结直肠癌组织中的表达水平显著低于癌旁组织（P＜0.05）,并与患者TNM分期和远处转移有关（均P＜0.05）;miR-23b-3p在结肠癌细胞系中的表达水平均显著低于FHC细胞,上调miR-23b-3p表达能显著抑制SW620细胞的侵袭和迁移能力。KLF3在结直肠癌组织和细胞中高表达,与miR-23b-3p在结直肠癌组织中的表达呈负相关（r=-0.326,P=0.013）,双荧光素酶报告基因实验证实miR-23b-3p直接靶向调节KLF3的表达, KLF3过表达能促进SW620细胞的侵袭和迁移,同时转染miR-23b-3p mimics可下调KLF3蛋白和mRNA表达,逆转KLF3过表达对SW620细胞侵袭和迁移能力的促进作用。结论:miR-23b-3p在结直肠癌中低表达并与肿瘤患者TNM分期及远处转移相关,miR-23b-3p靶向调控KLF3表达抑制结直肠癌SW620细胞的侵袭和迁移能力。     

MiR-625-3p promotes cell migration and invasion via inhibition of SCAI in colorectal carcinoma cells

MicroRNAs (miRNAs) play a critical role in controlling tumor invasion and metastasis via regulating the expression of a variety of targets, which act as oncogenes or tumor suppressor genes. Abnormally expressed miR-625-3p has been observed in several types of human cancers. However, the molecular mechanisms of miR-625-3p-mediated tumorigenesis are largely elusive. Therefore, the aim of this study was to evaluate the biological function and molecular insight on miR-625-3p-induced oncogenesis in colorectal carcinoma (CRC). The effects of miR-625-3p in cell migration and invasion were analyzed by wound healing assay and transwell assay, respectively. In addition, the expression of miR-625-3p and its targets was detected in five human CRC cell lines. In the present study, we found that overexpression of miR-625-3p promoted migration and invasion in SW480 cells, whereas downregulation of miR-625-3p inhibited cell motility in SW620 cells. More importantly, we observed potential binding sites for miR-625-3p in the 3′-untranslated region of suppressor of cancer cell invasion (SCAI). Notably, we identified that overexpression of miR-625-3p inhibited the expression of SCAI, while depletion of miR-625-3p increased SCAI level, suggesting that SCAI could be a target of miR-625-3p. Additionally, we revealed that miR-625-3p exerts its oncogenic functions through regulation of SCAI/E-cadherin/MMP-9 pathways. Our findings indicate the pivotal role of miR-625-3p in invasion that warrants further exploration whether targeting miR-625-3p could be a promising approach for the treatment of CRC.     

Upregulation of miR-324-5p Inhibits Proliferation and Invasion of Colorectal Cancer Cells by Targeting ELAVL1

Colorectal cancer (CRC) is a common clinical cancer that remains incurable in most cases. miRNAs are reported to play a part in the development of various tumors. In the present study, we found that miR-324-5p was downregulated in CRC cells, while ELAV (embryonic lethal, abnormal vision, Drosophila)-like protein 1 (ELAVL1) showed a higher expression. miR-324-5p transfection significantly inhibited the proliferation as well as invasion in both SW620 and SW480 cells. miR-324-5p mimic transfection markedly decreased the expression of ELAVL1. Luciferase reporter gene assay confirmed that ELAVL1 is a direct target of miR- 324-5p. Furthermore, cancer invasion factors uPA, uPAR, and MMP-9 were found to drop significantly in miR-324-5p-transfected groups. To conclude, our findings indicate that miR-324-5p may play a suppressive role in colorectal cell viability and invasion, at least in part, through directly targeting ELAVL1. Therefore, miR-234-5p might function as a promising candidate for CRC treatment and deserves deeper research.     

lncRNASNHG10靶向调控miR-532-3p促进结直肠癌SW620细胞的侵袭和迁移

目的： 探讨lncRNA SNHG10在结直肠癌组织和细胞中的表达情况及其对结直肠癌细胞侵袭和迁移的影响与可能的机制。 方法： 收集2018年1月至2019年12月在河南省人民医院行根治性结直肠癌切除术的78例患者的癌组织及对应癌旁组织标本,采用qPCR法检测结直肠癌组织、结直肠癌细胞（SW480、SW620、HT-29和LoVo）及人正常结直肠黏膜细胞FHC中lncRNA SNHG10和miR-532-3p的表达水平,并分析其与结直肠癌患者临床病理特征的关系及在组织中表达的相关性。采用双荧光素酶报告基因实验验证lncRNA SNHG10和miR-532-3p间的靶向关系。向SW620细胞中转染si-SNHG10或miR-532-3p mimic或共转染si-SNHG10+miR-532-3p inhibitor,采用Transwell实验检测其侵袭和迁移能力的改变,采用WB法检测E-cadherin,N-cadherin和vimentin蛋白表达水平变化。 结果： SNHG10 在结直肠癌组织和细胞中呈高表达（P<0.05 或 P<0.01）,其表达水平与TNM分期和远处转移有关（均P<0.05）;miR-532-3p在结直肠癌组织和细胞中呈低表达,其表达水平与TNM分期、淋巴结转移和远处转移有关（P<0.05或P<0.01）,SNHG10和miR-532-3p在结直肠癌组织中的表达呈负相关（r=-0.225, P=0.048）。双荧光素酶报告基因实验证实SNHG10靶向调节miR-532-3p的表达。下调 SNHG10 或上调 miR-532-3p 的表达后,SW620 细胞的侵袭和迁移能力显著降低（P<0.01）,E-cadherin蛋白表达水平升高（P<0.05）、N-cadherin和vimentin蛋白表达水平降低（均P<0.05）。抑制miR-532-3p表达后,敲低lncRNA SNHG10表达对结直肠癌细胞侵袭和迁移的抑制作用被逆转（均P<0.05）。 结论： lncRNA SNHG10在结直肠癌中高表达并与TNM分期和远处转移相关,lncRNASNHG10靶向调控miR-532-3p表达并通过EMT途径影响结直肠癌细胞的侵袭和转移。     

结直肠癌中 RhoGDI2的表达与肿瘤侵袭、转移及预后的关系

目的：探讨 RhoGDI2在结直肠癌中的表达与肿瘤侵袭、转移及预后的关系。方法：应用 Northern blot和 Western blot 检测具有不同侵袭、转移潜能的人结直肠癌细胞系（SW620、SW480）中 RhoGDI2 mRNA 及蛋白的表达。收集行手术切除并随访满5年的结直肠癌患者原发灶癌组织石蜡标本80例及相应的癌旁非癌组织、转移性淋巴结癌组织石蜡标本各20例。应用免疫组化法检测上述120例标本中 RhoGDI2蛋白的表达,分析其与临床病理特征及预后的关系。结果：SW620、SW480人结直肠癌细胞系中 RhoGDI2 mRNA 及蛋白的表达具有统计学差异（P <0.01）,前者表达均高于后者。结直肠癌相关组织中 RhoGDI2蛋白存在差异性表达（转移淋巴结癌组织>原发灶癌组织>癌旁非癌组织,P <0.01）。RhoGDI2蛋白在结直肠癌组织中的表达与肿瘤的浸润深度、淋巴结转移、远处转移、周围淋巴管浸润、周围神经浸润、TNM 分期显著相关（P <0.05）。RhoGDI2高表达的结直肠癌患者5年生存率显著低于低表达者（P <0.01）。高 RhoGDI2表达是结直肠癌的独立预后因素之一（P <0.05）。结论：RhoGDI2在结直肠癌中的高表达与肿瘤的侵袭、转移及预后不良密切相关,可能是一个有效的结直肠癌预后标志物。     

转凝蛋白在结直肠癌组织中的表达及其对SW480细胞恶性生物学行为的影响

目的:探讨转凝蛋白(transgelin,TAGLN)在结直肠癌(colorectal cancer,CRC)组织中的表达及其对SW480细胞增殖、迁移及侵袭的影响.方法:选取郑州大学附属肿瘤医院2015年5月至2016年8月收治的97例CRC患者的癌及配对的癌旁组织标本,以及人CRC细胞系SW620、SW480、HC...     

The expression and the functional roles of tissue factor and protease-activated receptor-2 on SW620 cells

Tissue factor (TF) is believed to play an important role in tissue repair, inflammation, angiogenesis, and tumor metastasis. Protease-activated receptors (PARs) are widely expressed on various cells including tumor cells and associated with many pathological mechanisms. In the present study, the expression of TF and PAR1, PAR2 on human colon cancer cells (SW620 and SW480) was investigated and their functional roles on the behavior of tumor cells were evaluated. It was demonstrated that SW620 and SW480 cells expressed TF at antigen, activity and mRNA levels. However, the highly metastatic cell line SW620 showed slightly higher TF expression than the low metastatic cell line SW480. The PAR2 antigen was strongly expressed on the membrane of SW620 cells, but not on SW480 cells. The PAR1 antigen was not observed in SW620 or SW480 cells, while PAR1 and PAR2 mRNA was detected in SW620 and SW480 cells. The migratory potential of SW620 was stronger than that of SW480 seen in Boyden chambers. PAR2 agonist (SLIGKV-NH2) and factor VIIa significantly stimulated SW620 cell proliferation, migratory activity, and interleukin 8 (IL-8) secretion compared to control. The stimulating effects of factor VIIa could be inhibited by anti-TF and anti-PAR2 but not anti-PAR1 antibodies. In summary, this study demonstrates that TF and PAR2 are strongly expressed on highly metastatic colonic tumor cells and are closely associated with the proliferation and migration of the cells. TF may elucidate its roles in colonic cancer invasion and metastasis via PAR2 pathway.     

miR-33a通过下调lumican基因抑制结肠癌细胞的侵袭和迁移

目的:探讨不同级别结肠癌中miR-33a和基膜聚糖(lumican)基因的表达情况,同时研究miR-33a对于结肠癌细胞侵袭和迁移的影响.方法:收集2015年1月至2016年1月新乡医学院第一附属医院肿瘤科收治的141例结肠癌患者,Western blotting和qPCR检测不同级别结肠癌组织中miR-33a和lumican的表达情况.使用miR-33a mimic转染人结肠癌细胞SW480,qPCR检测miR-33a mimic转染后细胞miR-33a和lumican mRNA的表达变化情况,使用Transwell侵袭实验检测miR-33a对人结肠癌细胞SW480侵袭能力的影响,使用划痕实验检测miR-33a对人结肠癌细胞SW480迁移能力的影响.裸鼠皮下成瘤实验检测miR-33a对结肠癌移植瘤生长以及裸鼠生存的影响.结果:随着结肠癌肿瘤级别的增加,miR-33a表达明显降低,而lumican表达水平明显增加;随着结肠癌病理分期和分级的增加,miR-33a表达逐渐降低;淋巴结转移的结肠癌组织中miR-33a的表达明显降低.转染miR-33a-mimic可以明显上调miR-33a的表达,上调miR-33a可以显著降低lumican蛋白表达水平、可以抑制结肠癌细胞的侵袭和迁移能力.miR-33a-mimic组荷瘤裸鼠肿瘤增长幅度明显减慢,而荷瘤裸鼠生存期明显延长.结论:miR-33a与结肠癌分期、分级以及是否有淋巴结转移有关,miR-33a可通过下调lumican抑制结肠癌细胞的侵袭和迁移.     

MiRNA-10a is upregulated in NSCLC and may promote cancer by targeting PTEN

MicroRNAs (miRNAs) are involved in human cancer including non-small cell lung cancer (NSCLC). In this study, we compared miRNA expression microarray of SPC-A-1sci (high metastatic) and SPC-A-1 (weakly metastatic) cells. We found that miRNA-10a was up-regulated in NSCLC compared with corresponding normal tissues. High expression of miR-10a was associated with tumor node metastasis and lymph node metastasis. Furthermore, overexpression of miR-10a promoted NSCLC cell proliferation, migration and invasion in vitro. We found that PTEN was a direct target of miR-10a in NSCLC. Also miR-10a activated the PTEN/AKT/ERK pathway. We suggest that miR-10a contributes to NSCLC by targeting PTEN.     

microRNA-320a inhibits tumor invasion by targeting neuropilin 1 and is associated with liver metastasis in colorectal cancer

MicroRNAs (miRNAs) have been implicated in regulating diverse cellular pathways. Although there is emerging evidence that various miRNAs function as oncogenes or tumor suppressors in colorectal cancer (CRC), the role of miRNAs in mediating liver metastasis remains unexplored. The expression profile of miRNAs in liver metastasis and primary CRC tissues was analyzed by miRNA microarrays and verified by real-time polymerase chain reaction (PCR). In 62 CRC patients, the expression levels of miR-320a were determined by real-time PCR, and the effects on migration and invasion of miR-320a were determined using a transwell assay. miR-320a target genes were confirmed by luciferase assay, real-time PCR and western blot analysis. A set of miRNAs was found to be dysregulated in the liver metastasis tissues compared to matched primary CRC tissues, and the expression levels of miR-320a were significantly decreased in the liver metastasis tissues examined. miR-320a was correlated with tumor progression in CRC. miR-320a was downregulated in liver metastatic colon cancer cells and inhibited liver metastatic colon cancer cell migration and invasion. miR-320a directly binds to the 3'UTR of neuropilin 1 (NRP-1), a protein that functions as a co-receptor of vascular epithelial growth factor. miR-320a downregulated the expression of NRP-1 at both the mRNA and protein levels. These data demonstrated that miR-320a may be useful for identifying CRC patients that are at an elevated risk for developing liver metastasis. Our findings suggest that miR-320a may be a novel therapeutic candidate for the treatment of colorectal cancer.     

MiR-150-5p Suppresses Colorectal Cancer Cell Migration and Invasion through Targeting MUC4

Growing evidence suggests that miR-150-5p has an important role in regulating genesis of various types of cancer. However, the roles and the underlying mechanisms of miR-150-5p in development of colorectal cancer (CRC) remain largely unknown. Transwell chambers were used to analyze effects on cell migration and invasion by miR-150-5p. Quantitative real-time PCR (qRT-PCR), Western blotting and dual-luciferase 3’ UTR reporter assay were carried out to identify the target genes of miR-150-5p. In our research, miR-150-5p suppressed CRC cell migration and invasion, and MUC4 was identified as a direct target gene. Its effects were partly blocked by re-expression of MUC4. In conclusiomn, miR-150-5p may suppress CRC metastasis through directly targeting MUC4, highlighting its potential as a novel agent for the treatment of CRC metastasis.     

The leukocyte protein L-plastin induces proliferation, invasion and loss of E-cadherin expression in colon cancer cells

L-plastin, a gene that codes for an actin-bundling protein, is upregulated in the metastatic colon cancer cell line SW620, when compared to its premetastatic counterpart SW480. The aim of our study was to characterise the effect of L-plastin overexpression on SW480 cells in the context of the acquisition of a metastatic phenotype. SW480 cell lines overexpressing L-plastin were established (SW480-LPL). Analysis of these cell lines revealed significantly higher rates of proliferation and invasion than the control cell line (SW480-Ctrl). In addition, the expression of E-cadherin was lost from SW480-LPL cells. Treatment of SW480-LPL cells with cytochalasin B, an inhibitor of endocytosis, attenuated the loss of E-cadherin expression in these cells. The association of L-plastin overexpression with an increased rate of proliferation and invasion, and loss of E-cadherin expression in the SW480 colon cancer cell line indicates that L-plastin plays an important mechanistic role in colorectal cancer metastasis (supplementary material for this article can be found on the International Journal of Cancer website at http://www.interscience.wiley.com/jpages/0020-7136/suppmat/index.html).     

miR-103/107 promote metastasis of colorectal cancer by targeting the metastasis suppressors DAPK and KLF4

Metastasis is the major cause of poor prognosis in colorectal cancer (CRC), and increasing evidence supports the contribution of miRNAs to cancer progression. Here, we found that high expression of miR-103 and miR-107 (miR-103/107) was associated with metastasis potential of CRC cell lines and poor prognosis in patients with CRC. We showed that miR-103/107 targeted the known metastasis suppressors death-associated protein kinase (DAPK) and Krüppel-like factor 4 (KLF4) in CRC cells, resulting in increased cell motility and cell-matrix adhesion and decreased cell-cell adhesion and epithelial marker expression. miR-103/107 expression was increased in the presence of hypoxia, thereby potentiating DAPK and KLF4 downregulation and hypoxia-induced motility and invasiveness. In mouse models of CRC, miR-103/107 overexpression potentiated local invasion and liver metastasis effects, which were suppressed by reexpression of DAPK or KLF4. miR-103/107-mediated downregulation of DAPK and KLF4 also enabled the colonization of CRC cells at a metastatic site. Clinically, the signature of a miR-103/107 high, DAPK low, and KLF4 low expression profile correlated with the extent of lymph node and distant metastasis in patients with CRC and served as a prognostic marker for metastasis recurrence and poor survival. Our findings therefore indicate that miR-103/107-mediated repression of DAPK and KLF4 promotes metastasis in CRC, and this regulatory circuit may contribute in part to hypoxia-stimulated tumor metastasis. Strategies that disrupt this regulation might be developed to block CRC metastasis.     

NUBPL,a novel metastasis‐related gene,promotes colorectal carcinoma cell motility by inducing epithelial–mesenchymal transition

Nucleotide binding protein‐like, NUBPL, is an assembly factor for human mitochondrial complex I, which is the biggest member of the mitochondrial respiratory chain. However, the relationship between NUBPL and carcinoma progression remains unknown. In this study, NUBPL was characterized for its role in colorectal cancer (CRC) and the underlying molecular mechanisms. Data (n = 197) from the Oncomine database revealed that mRNA levels of NUBPL were remarkably overexpressed in CRC tissues compared with normal tissues. In addition, immunohistochemical analysis of 75 pairs of CRC and non‐tumor tissues showed that the expression level of NUBPL was significantly higher in CRC tissues, and its expression level was positively associated with lymph node metastasis (P = 0.028) and advanced staging (P = 0.030). Expression of NUBPL in metastatic lymph nodes of CRC patients was also detected by immunohistochemical staining and high expression levels of NUBPL were observed. Overexpression of NUBPL significantly promoted the migration and invasion ability of CRC cell lines SW480 and SW620, whereas knockdown of NUBPL lead to an opposite effect. Our further study found that NUBPL could induce epithelial–mesenchymal transition (EMT), characterized by downregulation of epithelial markers (E‐cadherin) and upregulation of mesenchymal markers (N‐cadherin and vimentin). Moreover, NUBPL was able to activate ERK, which is believed to promote EMT and tumor metastasis. Inhibition of ERK suppressed the NUBPL‐induced changes in EMT and cell motility. These data showed that NUBPL plays a vital role in CRC migration and invasion by inducing EMT and activating ERK. It might be a novel therapeutic target for CRC.     

Primary tumor- and metastasis-derived colon cancer cells differently modulate connexin expression and function in human capillary endothelial cells

A gradual loss of functional gap junction between tumor cells has been reported with colorectal cancer (CRC) progression. Here, we explored if colon cancer cells could also affect gap junctions in blood capillary cells. Human microvascular endothelial cells (HMEC) were cultured with two CRC cell lines established from a unique patient. SW480 cells, derived from the primary tumor, migrate much faster across HMEC monolayer than SW620 cells derived from a metastatic site. The motile SW480 cells highly express and release HSP27 that increases gap junction formation with HMEC. Soluble HSP27 phosphorylates the connexin Cx43 on serine residues and induces its interaction with the oncoprotein 14-3-3, which promotes Cx43 delivery at the plasma membrane. The factors secreted by less motile SW620 cells do not affect Cx43 expression but up-regulate the expression of the connexin Cx32 through an activation of the chemokine receptor CXCR2. In turn, SW620 secreted factors induce tubulogenesis and ATP release. Altogether, cell lines derived from CRC primary tumor and metastasis differentially adapt endothelial cell functions by modulating connexin expression through released mediators.     

miR-21 functionally interacts with the 3'UTR of chemokine CCL20 and down-regulates CCL20 expression in miR-21 transfected colorectal cancer cells

As deregulation of miRNAs and chemokine CCL20 was shown to play a role in colorectal cancer (CRC) pathogenesis, we analyzed the functional interactions of candidate miRNAs with CCL20 mRNA. After target prediction software programs indicated a role for miR-21 in CCL20 regulation, we applied the luciferase reporter assay system to demonstrate that miR-21 functionally interacts with the 3′UTR of CCL20 mRNA and down-regulates CCL20 in miR-21 mimic transfected CRC cell lines (Caco-2, SW480 and SW620). Thus, regulation of CCL20 expression by miR-21 might be a regulatory mechanism involved in progression of CRC.     

Astrocyte elevated gene‐1 interacts with β‐catenin and increases migration and invasion of colorectal carcinoma

To investigate the astrocyte elevated gene‐1 (AEG‐1) expression and its relationship with the clinicopathological features of colorectal carcinoma (CRC) and β‐catenin signaling pathway. Real‐time PCR, Western blot, immunohistochemistry, and immunofluorescence staining were performed to detect AEG‐1 expression in CRC cell lines, 8 pairs of fresh CRC and adjacent nontumor tissues (ANT), 120 pairs of paraffin‐embedded CRC specimens and ANT tissues, and 60 samples of lymph node metastatic CRC tissues. Scratch wound assay and transwell matrix penetration assay were performed to determine migration and invasion of SW480 cell lines with stable AEG‐1 overexpression or SW620 cell lines with AEG‐1 knockdown. AEG‐1 expression was upregulated in CRC cell lines and tissues compared with ANT. Furthermore, AEG‐1 expression level significantly correlated with UICC stage, and the N classification. AEG‐1 overexpression significantly enhanced migration and invasion of SW480 cell lines. However, AEG‐1 knockdown suppressed migration and invasion of SW620 cell lines. Meanwhile, there was a positive correlation between AEG‐1 high expression and β‐catenin nuclear expression in CRC. AEG‐1 overexpression increased nuclear β‐catenin accumulation in CRC cell lines. AEG‐1 knockdown decreased nuclear β‐catenin accumulation in CRC cell lines. Moreover, we firstly found that AEG‐1 interacted with β‐catenin in SW480 cell lines. Our results for the first time showed that AEG‐1 interacted with β‐catenin in CRC cells and AEG‐1 expression was closely associated with progression of CRC. AEG‐1 might be a potential therapeutic target in CRC. © 2012 Wiley Periodicals, Inc.