Post-transcriptional mechanisms contribute to the suppression of the ErbB3 negative regulator protein Nrdp1 in mammary tumors.

The Journal of Biological Chemistry
Ellen Q IngallaKermit L Carraway

Abstract

The ErbB2 and ErbB3 receptor tyrosine kinases act synergistically to promote cellular properties associated with tumor development. Previous studies indicate that endogenous ErbB3 protein is markedly elevated in mouse mammary tumors induced by transgenic ErbB2 overexpression. However, this occurs in the absence of elevated ErbB3 transcript, indicating that post-transcriptional regulatory mechanisms play crucial roles in suppressing ErbB3 protein in normal tissue. Our previous studies also demonstrate that protein levels of Nrdp1, an E3 ubiquitin ligase that targets ErbB3 for degradation, are markedly suppressed in tumors from ErbB2 transgenic animals relative to normal tissue. Here we demonstrate that transgenic expression of Nrdp1 cDNA in the mouse mammary gland is not sufficient to suppress elevated ErbB3 levels or tumor initiation and growth in ErbB2 transgenic mice. Unexpectedly, Nrdp1 protein is absent in tumors from Nrdp1/ErbB2 bigenic mice, and real time PCR analysis indicates that Nrdp1 protein levels are suppressed post-transcriptionally. Nrdp1 protein is more resistant to proteasome-dependent degradation when exogenously expressed in cultured MCF10A nontransformed human breast epithelial cells than in breast tumor cel...Continue Reading

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Citations

May 18, 2011·Molecular and Cellular Biology·William H D FryKermit L Carraway
Mar 8, 2011·Journal of Cell Science·Joris WaumanJan Tavernier
Sep 28, 2010·Seminars in Cell & Developmental Biology·Kermit L Carraway
Dec 3, 2014·Nuclear Medicine and Biology·Jai Woong SeoKatherine W Ferrara
Nov 18, 2014·Oncotarget·Kalpana MujooZhiqiang An
Nov 18, 2017·BMC Biology·Sara Sannino, Jeffrey L Brodsky
Jun 21, 2020·Cell Biochemistry and Biophysics·Yong LiuChengmin Xuan
Jun 5, 2021·Lung Cancer Management·Thubeena ManickavasagarAnna Minchom
Mar 22, 2018·Journal of Proteome Research·Delphine MasschaeleJan Tavernier

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