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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

Increased expression of ATF3 inhibits ESCC cell proliferation and motility. Overexpression of ATF3 by transfection with ATF3 expression plasmid inhibited (A) EC109 and (B) KYSE450 cell proliferation after 36 and 48 h compared with the cells transfected with the empty vector (*P<0.05 vs. empty vector). (C) Wound healing assay determined that the overexpression of ATF3 inhibited cell motility. ATF3, activating transcription factor 3; OD, optical density.
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f2-ol-0-0-4832: Increased expression of ATF3 inhibits ESCC cell proliferation and motility. Overexpression of ATF3 by transfection with ATF3 expression plasmid inhibited (A) EC109 and (B) KYSE450 cell proliferation after 36 and 48 h compared with the cells transfected with the empty vector (*P<0.05 vs. empty vector). (C) Wound healing assay determined that the overexpression of ATF3 inhibited cell motility. ATF3, activating transcription factor 3; OD, optical density.

Mentions: To determine the roles of ATF3 in ESCC cells, the ATF3 overexpression plasmid was transfected in to the EC109 and KYSE450 cells. It was observed that increased ATF3 expression significantly inhibited cell proliferation in each ESCC cell line (Fig. 2A and B). Wound healing assay demonstrated that ATF3 overexpression inhibited ESCC cell motility (Fig. 2C), and Transwell assay determined that ATF3 significantly inhibited ESCC cell migration (P<0.05) (Fig. 3).


ATF3 suppresses ESCC via downregulation of ID1
Increased expression of ATF3 inhibits ESCC cell proliferation and motility. Overexpression of ATF3 by transfection with ATF3 expression plasmid inhibited (A) EC109 and (B) KYSE450 cell proliferation after 36 and 48 h compared with the cells transfected with the empty vector (*P<0.05 vs. empty vector). (C) Wound healing assay determined that the overexpression of ATF3 inhibited cell motility. ATF3, activating transcription factor 3; OD, optical density.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998220&req=5

f2-ol-0-0-4832: Increased expression of ATF3 inhibits ESCC cell proliferation and motility. Overexpression of ATF3 by transfection with ATF3 expression plasmid inhibited (A) EC109 and (B) KYSE450 cell proliferation after 36 and 48 h compared with the cells transfected with the empty vector (*P<0.05 vs. empty vector). (C) Wound healing assay determined that the overexpression of ATF3 inhibited cell motility. ATF3, activating transcription factor 3; OD, optical density.
Mentions: To determine the roles of ATF3 in ESCC cells, the ATF3 overexpression plasmid was transfected in to the EC109 and KYSE450 cells. It was observed that increased ATF3 expression significantly inhibited cell proliferation in each ESCC cell line (Fig. 2A and B). Wound healing assay demonstrated that ATF3 overexpression inhibited ESCC cell motility (Fig. 2C), and Transwell assay determined that ATF3 significantly inhibited ESCC cell migration (P<0.05) (Fig. 3).

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&lt;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