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Article

Disruption of the RP-MDM2-p53 pathway accelerates APC loss-induced colorectal tumorigenesis.

Oncogene - 1 Mar 2017

Liu S, Tackmann N R, Yang J, Zhang Y

Abstract excerpt

Inactivation of the adenomatous polyposis coli (APC) tumor suppressor is frequently found in colorectal cancer. Loss of APC function results in deregulation of the Wnt/β-catenin signaling pathway causing overexpression of the c-MYC oncogene. In lymphoma, both p19ARF and ribosomal proteins RPL11 and RPL5 respond to c-MYC activation to induce p53. Their role in c-MYC-driven colorectal carcinogenesis is unclear, as...

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Topics

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Share to Adenomatous Polyposis Coli
Share to Cell Transformation, Neoplastic
Share to Colorectal Neoplasms

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Intestinal Mucosa

Share to Proto-Oncogene Proteins c-mdm2

Share to Proto-Oncogene Proteins c-myc

Share to Ribosomal Proteins

Share to Tumor Suppressor Protein p53

Source

Open in PubMed Open full text

Identifiers

PMID: 27617574
DOI: 10.1038/onc.2016.301
PMCID: PMC5693310

Genes

APC
MDM2
MYC
RPL11
RPL5

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Disruption of the RP-MDM2-p53 pathway accelerates APC loss-induced colorectal tumorigenesis.PMID 27617574Read ↗

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