Role of TET1 inhibition in IL-1 augmentation of TGF-B induced Epithelial to Mesenchymal transition in A549 lung adenocarcinoma cells
Location
Philadelphia, PA
Start Date
17-4-2026 1:30 PM
End Date
17-4-2026 2:30 PM
Description
Introduction: Lung cancer is one of the leading causes of cancer death worldwide. Epithelial-mesenchymal transition (EMT) plays a role in the fatality of lung cancer by decreasing epithelial characteristics and allowing for migration and invasion. IL-1 enhances TGF-β induced EMT in A549 lung adenocarcinoma cells. Previous experiments showed that IL-1 inhibits the induction of Ten-eleven-translocation-1 (TET1) by TGF-β and this is accompanied by additive inhibition of E-cadherin expression. TET1 is known to have a role in inhibiting the expression of zinc-finger- Ebox binding homeobox 1 (ZEB1), a repressor of E-cadherin. Additionally, SNAI1 (Snail) and SNAI2 (Slug) are Zinc-finger transcription factors that suppress E-cadherin. The current series of experiments aims to determine whether the inhibition of TET1 activity can enhance TGF-β induced EMT similarly to IL1.
Methods: Real time qPCR was used to examine mRNA expression in A549 cells in response to IL1 and TGF-β in the presence and absence of Bobcat339, a TET1 inhibitor.
Results: Although IL-1 does enhance TGF-β induced expression of ZEB1 mRNA at 3 and 6 hours, inhibition of TET1 activity did not affect ZEB1 mRNA expression.
Conclusion: Previous data suggested that inhibition of TET1 activity might play at least a partial role in IL-1 enhancement of TGF- β induced EMT. However, if TET1 inhibition is involved in EMT enhancement, the current data suggests that it is unlikely to be mediated by TET1 enzymatic effects. Future experiments will explore the possibility that TET1 influences ZEB1 expression, and therefore EMT, via a non-enzymatic mechanism.
Embargo Period
5-20-2026
Role of TET1 inhibition in IL-1 augmentation of TGF-B induced Epithelial to Mesenchymal transition in A549 lung adenocarcinoma cells
Philadelphia, PA
Introduction: Lung cancer is one of the leading causes of cancer death worldwide. Epithelial-mesenchymal transition (EMT) plays a role in the fatality of lung cancer by decreasing epithelial characteristics and allowing for migration and invasion. IL-1 enhances TGF-β induced EMT in A549 lung adenocarcinoma cells. Previous experiments showed that IL-1 inhibits the induction of Ten-eleven-translocation-1 (TET1) by TGF-β and this is accompanied by additive inhibition of E-cadherin expression. TET1 is known to have a role in inhibiting the expression of zinc-finger- Ebox binding homeobox 1 (ZEB1), a repressor of E-cadherin. Additionally, SNAI1 (Snail) and SNAI2 (Slug) are Zinc-finger transcription factors that suppress E-cadherin. The current series of experiments aims to determine whether the inhibition of TET1 activity can enhance TGF-β induced EMT similarly to IL1.
Methods: Real time qPCR was used to examine mRNA expression in A549 cells in response to IL1 and TGF-β in the presence and absence of Bobcat339, a TET1 inhibitor.
Results: Although IL-1 does enhance TGF-β induced expression of ZEB1 mRNA at 3 and 6 hours, inhibition of TET1 activity did not affect ZEB1 mRNA expression.
Conclusion: Previous data suggested that inhibition of TET1 activity might play at least a partial role in IL-1 enhancement of TGF- β induced EMT. However, if TET1 inhibition is involved in EMT enhancement, the current data suggests that it is unlikely to be mediated by TET1 enzymatic effects. Future experiments will explore the possibility that TET1 influences ZEB1 expression, and therefore EMT, via a non-enzymatic mechanism.