Original Article
LncRNA-DANCR promotes growth and metastasis of colorectal cancer via activating epithelial-mesenchymal transition process
Abstract
Background: The aim of this study was to investigate the effects and underlying mechanism of long non- coding RNA-differentiation antagonizing non-protein coding RNA (lncRNA-DANCR) on colorectal cancer (CRC).
Methods: The expression of lncRNA-DANCR in CRC and pericarcinous tissues from 40 CRC patients, and the expression in HT-29 cells and FHC cells, were determined by qRT-PCR. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The migration and invasion of CRC cells were detected by wound healing assay and transwell assay, respectively. HT-29 cells were transfected and divided into three groups: BLANK group, si-NC group and si-DANCR group. After transfection, the expression of lncRNA-DANCR was detected by qRT-PCR. The expression of E-cadherin and vimentin was detected by western blot and immunofluorescence. The mice model of xenograft tumor was established and histological changes of lung lobes sections were measured by hematoxylin-eosin (HE) staining.
Results: The expression of lncRNA-DANCR in CRC tissues and HT-29 cells was significantly higher than that in non-CRC tissues and FHC cells. Silencing lncRNA-DANCR could significantly inhibit the proliferation, invasion and metastasis of HT-29 cells. Western blot showed that the expression of E-cadherin increased significantly and vimentin decreased significantly after silencing lncRNA-DANCR. The same results were observed in immunofluorescence experiment. Silence of lncRNA-DANCR markedly suppressed the growth and metastasis of CRC.
Conclusions: LncRNA-DANCR may facilitate the growth and metastasis of CRC by regulating the epithelial-mesenchymal transition (EMT) process.
Methods: The expression of lncRNA-DANCR in CRC and pericarcinous tissues from 40 CRC patients, and the expression in HT-29 cells and FHC cells, were determined by qRT-PCR. Cell proliferation was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The migration and invasion of CRC cells were detected by wound healing assay and transwell assay, respectively. HT-29 cells were transfected and divided into three groups: BLANK group, si-NC group and si-DANCR group. After transfection, the expression of lncRNA-DANCR was detected by qRT-PCR. The expression of E-cadherin and vimentin was detected by western blot and immunofluorescence. The mice model of xenograft tumor was established and histological changes of lung lobes sections were measured by hematoxylin-eosin (HE) staining.
Results: The expression of lncRNA-DANCR in CRC tissues and HT-29 cells was significantly higher than that in non-CRC tissues and FHC cells. Silencing lncRNA-DANCR could significantly inhibit the proliferation, invasion and metastasis of HT-29 cells. Western blot showed that the expression of E-cadherin increased significantly and vimentin decreased significantly after silencing lncRNA-DANCR. The same results were observed in immunofluorescence experiment. Silence of lncRNA-DANCR markedly suppressed the growth and metastasis of CRC.
Conclusions: LncRNA-DANCR may facilitate the growth and metastasis of CRC by regulating the epithelial-mesenchymal transition (EMT) process.
