BxPC3 pancreatic cancer cells express a truncated Smad4 protein upon PI3K and mTOR inhibition

Legendre,Onica; Sookdeo,Ayisha; Foster,David A.

doi:10.3892/ol.2014.1833

BxPC3 pancreatic cancer cells express a truncated Smad4 protein upon PI3K and mTOR inhibition

Authors:
- Onica Legendre
- Ayisha Sookdeo
- David A. Foster
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Affiliations: Department of Biological Sciences, Hunter College of The City University of New York, New York, NY 10065, USA
Published online on: January 28, 2014 https://doi.org/10.3892/ol.2014.1833
Pages: 1165-1168

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Abstract

Smad4 is a critical regulator of transforming growth factor (TGF)‑β signaling and is defective in numerous human cancers. In total, 30% of pancreatic cancers harbor a homozygous deletion of Smad4. The human pancreatic cancer cell line, BxPC3, has been reported to be Smad4‑null due to a homozygous deletion and has been widely used as a Smad4‑null model. The present study reports that Smad4 DNA is present in BxPC3 cells, and under conditions of suppressed mammalian target of rapamycin complex 1 (mTORC1) and phosphatidylinositol‑3‑kinase, a truncated Smad4 protein is expressed. While a high level of Smad4 protein can be expressed in these cells, the cells do not respond to TGF‑β. The Smad4 defect in BxPC3 cells likely occurs via translocation rather than deletion as previously reported.

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