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Dachshund Binds p53 to Block the Growth of Lung Adenocarcinoma Cells
Journal article   Open access   Peer reviewed

Dachshund Binds p53 to Block the Growth of Lung Adenocarcinoma Cells

Ke Chen, Kongming Wu, Shaoxin Cai, Wei Zhang, Jie Zhou, Jing Wang, Adam Ertel, Zhiping Li, Hallgeir Rui, Andrew Quong, …
Cancer research (Chicago, Ill.), v 73(11), pp 3262-3274
01 Jun 2013
PMID: 23492369
url
https://doi.org/10.1158/0008-5472.can-12-3191View
Accepted (AM)Open Access (License Unspecified) Open

Abstract

Life Sciences & Biomedicine Oncology Science & Technology
Hyperactive EGF receptor (EGFR) and mutant p53 are common genetic abnormalities driving the progression of non-small cell lung cancer (NSCLC), the leading cause of cancer deaths in the world. The Drosophila gene Dachshund (Dac) was originally cloned as an inhibitor of hyperactive EGFR alleles. Given the importance of EGFR signaling in lung cancer etiology, we examined the role of DACH1 expression in lung cancer development. DACH1 protein and mRNA expression was reduced in human NSCLC. Reexpression of DACH1 reduced NSCLC colony formation and tumor growth in vivo via p53. Endogenous DACH1 colocalized with p53 in a nuclear, extranucleolar location, and shared occupancy of -15% of p53-bound genes in ChIP sequencing. The C-terminus of DACH1 was necessary for direct p53 binding, contributing to the inhibition of colony formation and cell-cycle arrest. Expression of the stem cell factor SOX2 was repressed by DACH1, and SOX2 expression was inversely correlated with DACH1 in NSCLC. We conclude that DACH1 binds p53 to inhibit NSCLC cellular growth. (C) 2013 AACR.

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Collaboration types
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Web of Science research areas
Oncology
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