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AIM:To investigate the biological role and underlying mechanism of miR-132 in colorectal cancer(CRC)progression and invasion.METHODS:Quantitative RT-PCR analysis was used to examine the expression levels of miR-132 in five CRC cell lines(SW480,SW620,HCT116,HT29 and LoVo)and a normal colonic cell line NCM460,as well as in tumor tissues with or without metastases.The KaplanMeier method was used to analyze the prognostic significance of miR-132 in CRC patients.The biological effects of miR-132 were assessed in CRC cell lines using the transwell assay.Quantitative RT-PCR and western blot analyses were employed to evaluate the expression of miR-132 targets.The regulation of ZEB2 by miR-132was confirmed using the luciferase activity assay.RESULTS:miR-132 was significantly down-regulated in the CRC cell lines compared with the normal colonic cell line(P<0.05),as well as in the CRC tissues withdistant metastases compared with the tissues without metastases(10.52±4.69 vs 23.11±7.84)(P<0.001).Down-regulation of miR-132 was associated with tumor size(P=0.016),distant metastasis(P=0.002),and TNM stage(P=0.020)in CRC patients.Kaplan-Meier survival curve analysis indicated that patients with low expression of miR-132 tended to have worse diseasefree survival than patients with high expression of miR-132(P<0.001).Moreover,ectopic expression of miR-132 markedly inhibited cell invasion(P<0.05)and the epithelial-mesenchymal transition(EMT)in CRC cell lines.Further investigation revealed ZEB2,an EMT regulator,was a downstream target of miR-132.CONCLUSION:Our study indicated that miR-132 plays an important role in the invasion and metastasis of CRC.
AIM: To investigate the biological role and underlying mechanism of miR-132 in colorectal cancer (CRC) progression and invasion. METHODS: Quantitative RT-PCR analysis was used to examine the expression levels of miR-132 in five CRC cell lines (SW480, SW620, HCT116, HT29 and LoVo) and a normal colonic cell line NCM460, as well as in tumor tissues with or without metastases. The Kaplan Meier method was used to analyze the prognostic significance of miR-132 in CRC patients. The biological effects of miR -132 were assessed in CRC cell lines using the transwell assay. Quantitative RT-PCR and western blot analyzes were employed to evaluate the expression of miR-132 targets. The regulation of ZEB2 by miR-132 was confirmed using the luciferase activity assay .RESULTS: miR-132 was significantly down-regulated in the CRC cell lines compared with the normal colonic cell line (P <0.05), as well as in the tissues with distant metastases compared with the tissues without metastases (10.52 ± 4.69 vs 23.11 ± 7.84) (P <0.001). Down-regulation of miR-132 was associated with tumor size (P = 0.016), distant metastasis (P = 0.002), and TNM stage (P = 0.020) in CRC patients. Kaplan-Meier survival curve analysis indicated that patients with low expression of miR-132 tended to have worse disease free survival than patients with high expression of miR-132 (P <0.001) .Moreover, ectopic expression of miR-132 markedly inhibited cell invasion (P <0.05) and the epithelial-mesenchymal transition ) in CRC cell lines. Future investigation revealed ZEB2, an EMT regulator, was a downstream target of miR-132. CONCLUSION: Our study indicates that miR-132 plays an important role in the invasion and metastasis of CRC.