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ATF3 suppresses ESCC via downregulation of ID1

View Article: PubMed Central - PubMed

ABSTRACT

Esophageal cancer is one of the most prevalent forms of cancer and has a particularly high mortality rate due to early metastasis; however, the underlying mechanisms of its formation and progression remain unclear. The present study performed immunohistochemical analysis and observed that the expression of activating transcription factor 3 (ATF3) was reduced in esophageal squamous cell carcinoma (ESCC) in comparison with non-tumor adjacent tissues. By contrast, inhibitor of DNA binding 1 (ID1) was overexpressed in ESCC tissues, demonstrating an inverse correlation with ATF3 (P<0.01). In ESCC EC109 and KYSE450 cells lines, transfection with an ATF3-overexpression plasmid resulted in the inhibition of cell proliferation, motility and migration, which was associated with the induction of E-cadherin expression and inhibition of cyclin D1 and Twist. Notably, ATF3 exerted an inverse regulatory interaction with ID1. The results of the present study provide additional evidence of the tumor suppressive features of ATF3 and demonstrate a novel mechanism of ATF3-mediated inhibition of cancer metastasis in esophageal cancer.

No MeSH data available.


Related in: MedlinePlus

Co-immunoprecipitation assay demonstrated that ATF3 physically binds with ID1. ESCC cell line EC109 cells were transfected with the pFlag-ATF3 plasmid and harvested 48 h post-transfection. The cell lysate was pulled down by anti-flag antibodies and the immunocomplex was probed by anti-ID1 antibodies.
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f5-ol-0-0-4832: Co-immunoprecipitation assay demonstrated that ATF3 physically binds with ID1. ESCC cell line EC109 cells were transfected with the pFlag-ATF3 plasmid and harvested 48 h post-transfection. The cell lysate was pulled down by anti-flag antibodies and the immunocomplex was probed by anti-ID1 antibodies.

Mentions: To further investigate the interaction between ATF3 and ID1, co-immunoprecipitation assay was performed. Anti-Flag antibodies were used to pull down the immune-complex and anti-ID1 antibodies were used to probe the complex. As presented in Fig. 5, there was a strong band in the precipitated immune-complex, therefore suggesting that the ATF3 and ID1 proteins had bound together.


ATF3 suppresses ESCC via downregulation of ID1
Co-immunoprecipitation assay demonstrated that ATF3 physically binds with ID1. ESCC cell line EC109 cells were transfected with the pFlag-ATF3 plasmid and harvested 48 h post-transfection. The cell lysate was pulled down by anti-flag antibodies and the immunocomplex was probed by anti-ID1 antibodies.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
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getmorefigures.php?uid=PMC4998220&req=5

f5-ol-0-0-4832: Co-immunoprecipitation assay demonstrated that ATF3 physically binds with ID1. ESCC cell line EC109 cells were transfected with the pFlag-ATF3 plasmid and harvested 48 h post-transfection. The cell lysate was pulled down by anti-flag antibodies and the immunocomplex was probed by anti-ID1 antibodies.
Mentions: To further investigate the interaction between ATF3 and ID1, co-immunoprecipitation assay was performed. Anti-Flag antibodies were used to pull down the immune-complex and anti-ID1 antibodies were used to probe the complex. As presented in Fig. 5, there was a strong band in the precipitated immune-complex, therefore suggesting that the ATF3 and ID1 proteins had bound together.

View Article: PubMed Central - PubMed

ABSTRACT

Esophageal cancer is one of the most prevalent forms of cancer and has a particularly high mortality rate due to early metastasis; however, the underlying mechanisms of its formation and progression remain unclear. The present study performed immunohistochemical analysis and observed that the expression of activating transcription factor 3 (ATF3) was reduced in esophageal squamous cell carcinoma (ESCC) in comparison with non-tumor adjacent tissues. By contrast, inhibitor of DNA binding 1 (ID1) was overexpressed in ESCC tissues, demonstrating an inverse correlation with ATF3 (P<0.01). In ESCC EC109 and KYSE450 cells lines, transfection with an ATF3-overexpression plasmid resulted in the inhibition of cell proliferation, motility and migration, which was associated with the induction of E-cadherin expression and inhibition of cyclin D1 and Twist. Notably, ATF3 exerted an inverse regulatory interaction with ID1. The results of the present study provide additional evidence of the tumor suppressive features of ATF3 and demonstrate a novel mechanism of ATF3-mediated inhibition of cancer metastasis in esophageal cancer.

No MeSH data available.


Related in: MedlinePlus