Limits...
COUP-TFII regulates metastasis of colorectal adenocarcinoma cells by modulating Snail1.

Bao Y, Gu D, Feng W, Sun X, Wang X, Zhang X, Shi Q, Cui G, Yu H, Tang C, Deng A - Br. J. Cancer (2014)

Bottom Line: Overexpression of COUP-TFII was required for cancer cells to metastasise in vivo.Chicken ovalbumin upstream promoter-transcription factor II regulated the transcription and expression of Snail1 by directly targeting the Snail1 promoter and regulated associated genes.Chicken ovalbumin upstream promoter-transcription factor II was found to be a biomarker associated with patient survival and colorectal cancer metastasis.

View Article: PubMed Central - PubMed

Affiliation: First Affiliated Hospital, Huzhou Teachers College, the First People's Hospital of Huzhou, Huzhou 313000, China.

ABSTRACT

Background: Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII, also known as NR2F2) promotes metastasis by functioning in the tumour microenvironment; however, the role of COUP-TFII in colorectal cancer remains unknown.

Methods: Human colon adenocarcinoma tissues were collected to test COUP-TFII expression. Wound-healing and cell invasion assay were used to evaluate migration and invasion of cells. Chicken ovalbumin upstream promoter-transcription factor II and related protein expression was assessed by immunostaining, immunoblotting and real-time PCR assay. Tamoxifen-inducible COUP-TFII knockout mice were employed to test COUP-TFII functions on colon cancer metastasis in vivo.

Results: Elevated expression of COUP-TFII in colorectal adenocarcinoma tissue correlated with overexpression of the Snail1 transcription factor. High COUP-TFII expression correlated with metastasis and shorter patient survival. Chicken ovalbumin upstream promoter-transcription factor II regulated the migration and invasion of cancer cells. With Snail1, COUP-TFII inhibited expression of adherence molecules such as ZO-1, E-cadherin and β-catenin in colorectal cancer cells. Overexpression of COUP-TFII was required for cancer cells to metastasise in vivo. Chicken ovalbumin upstream promoter-transcription factor II regulated the transcription and expression of Snail1 by directly targeting the Snail1 promoter and regulated associated genes.

Conclusions: Chicken ovalbumin upstream promoter-transcription factor II was crucial for colorectal cancer metastasis and regulated cell migration and metastasis in conjunction with Snail1. Chicken ovalbumin upstream promoter-transcription factor II was found to be a biomarker associated with patient survival and colorectal cancer metastasis.

Show MeSH

Related in: MedlinePlus

Chicken ovalbumin upstream promoter-transcription factor II regulation of colon cancer cell invasion is dependent on Snail1. Human colon adenocarcinoma LOVO or HT29 cells were transfected and cultured as described in Figure 1E. (A and B) Wound-healing assay with LOVO or HT29 cells transfected with indicated vectors showing wound width and percent closure of the original wound from triplicate plates. *P<0.01 compared to the same time points for control non-transfected (CON) wounded LOVO or HT29 cells. (C and D) LOVO or HT29 cells transfected with indicated vectors that penetrated Matrigel-coated filters. Quantitation is the mean number of cells in 10 random microscope fields. Data are mean±s.d., n=3; *P<0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4150277&req=5

fig2: Chicken ovalbumin upstream promoter-transcription factor II regulation of colon cancer cell invasion is dependent on Snail1. Human colon adenocarcinoma LOVO or HT29 cells were transfected and cultured as described in Figure 1E. (A and B) Wound-healing assay with LOVO or HT29 cells transfected with indicated vectors showing wound width and percent closure of the original wound from triplicate plates. *P<0.01 compared to the same time points for control non-transfected (CON) wounded LOVO or HT29 cells. (C and D) LOVO or HT29 cells transfected with indicated vectors that penetrated Matrigel-coated filters. Quantitation is the mean number of cells in 10 random microscope fields. Data are mean±s.d., n=3; *P<0.01.

Mentions: To study the effect of COUP-TFII on cell motility, we used an in vitro wound-healing assay, measuring the extent of cell migration into a scratched area. Migration of LOVO and HT29 cells was inhibited in cells in which COUP-TFII or Snail1 expression was repressed using shRNA. Migration inhibition was partially rescued by overexpression of Snail1 in COUP-TFII knockdown cells (Figure 2A and B). Moreover, the migration distance was decreased when Snail1 was depleted even in COUP-TFII overexpression cells.


COUP-TFII regulates metastasis of colorectal adenocarcinoma cells by modulating Snail1.

Bao Y, Gu D, Feng W, Sun X, Wang X, Zhang X, Shi Q, Cui G, Yu H, Tang C, Deng A - Br. J. Cancer (2014)

Chicken ovalbumin upstream promoter-transcription factor II regulation of colon cancer cell invasion is dependent on Snail1. Human colon adenocarcinoma LOVO or HT29 cells were transfected and cultured as described in Figure 1E. (A and B) Wound-healing assay with LOVO or HT29 cells transfected with indicated vectors showing wound width and percent closure of the original wound from triplicate plates. *P<0.01 compared to the same time points for control non-transfected (CON) wounded LOVO or HT29 cells. (C and D) LOVO or HT29 cells transfected with indicated vectors that penetrated Matrigel-coated filters. Quantitation is the mean number of cells in 10 random microscope fields. Data are mean±s.d., n=3; *P<0.01.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4150277&req=5

fig2: Chicken ovalbumin upstream promoter-transcription factor II regulation of colon cancer cell invasion is dependent on Snail1. Human colon adenocarcinoma LOVO or HT29 cells were transfected and cultured as described in Figure 1E. (A and B) Wound-healing assay with LOVO or HT29 cells transfected with indicated vectors showing wound width and percent closure of the original wound from triplicate plates. *P<0.01 compared to the same time points for control non-transfected (CON) wounded LOVO or HT29 cells. (C and D) LOVO or HT29 cells transfected with indicated vectors that penetrated Matrigel-coated filters. Quantitation is the mean number of cells in 10 random microscope fields. Data are mean±s.d., n=3; *P<0.01.
Mentions: To study the effect of COUP-TFII on cell motility, we used an in vitro wound-healing assay, measuring the extent of cell migration into a scratched area. Migration of LOVO and HT29 cells was inhibited in cells in which COUP-TFII or Snail1 expression was repressed using shRNA. Migration inhibition was partially rescued by overexpression of Snail1 in COUP-TFII knockdown cells (Figure 2A and B). Moreover, the migration distance was decreased when Snail1 was depleted even in COUP-TFII overexpression cells.

Bottom Line: Overexpression of COUP-TFII was required for cancer cells to metastasise in vivo.Chicken ovalbumin upstream promoter-transcription factor II regulated the transcription and expression of Snail1 by directly targeting the Snail1 promoter and regulated associated genes.Chicken ovalbumin upstream promoter-transcription factor II was found to be a biomarker associated with patient survival and colorectal cancer metastasis.

View Article: PubMed Central - PubMed

Affiliation: First Affiliated Hospital, Huzhou Teachers College, the First People's Hospital of Huzhou, Huzhou 313000, China.

ABSTRACT

Background: Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII, also known as NR2F2) promotes metastasis by functioning in the tumour microenvironment; however, the role of COUP-TFII in colorectal cancer remains unknown.

Methods: Human colon adenocarcinoma tissues were collected to test COUP-TFII expression. Wound-healing and cell invasion assay were used to evaluate migration and invasion of cells. Chicken ovalbumin upstream promoter-transcription factor II and related protein expression was assessed by immunostaining, immunoblotting and real-time PCR assay. Tamoxifen-inducible COUP-TFII knockout mice were employed to test COUP-TFII functions on colon cancer metastasis in vivo.

Results: Elevated expression of COUP-TFII in colorectal adenocarcinoma tissue correlated with overexpression of the Snail1 transcription factor. High COUP-TFII expression correlated with metastasis and shorter patient survival. Chicken ovalbumin upstream promoter-transcription factor II regulated the migration and invasion of cancer cells. With Snail1, COUP-TFII inhibited expression of adherence molecules such as ZO-1, E-cadherin and β-catenin in colorectal cancer cells. Overexpression of COUP-TFII was required for cancer cells to metastasise in vivo. Chicken ovalbumin upstream promoter-transcription factor II regulated the transcription and expression of Snail1 by directly targeting the Snail1 promoter and regulated associated genes.

Conclusions: Chicken ovalbumin upstream promoter-transcription factor II was crucial for colorectal cancer metastasis and regulated cell migration and metastasis in conjunction with Snail1. Chicken ovalbumin upstream promoter-transcription factor II was found to be a biomarker associated with patient survival and colorectal cancer metastasis.

Show MeSH
Related in: MedlinePlus