ArticleMolecular and cellular biology2018
Truncated Adenomatous Polyposis Coli Mutation Induces Asef-Activated Golgi Fragmentation.
Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 17 citations in OpenAlex.
- Article
- Truncated APC impairs innate immune response by targeting MAVS on mitochondria in colorectal cancer.Journal of translational medicine · 2025Article
- A truncation mutant of adenomatous polyposis coli impairs apical cell extrusion through elevated epithelial tissue tension.Cytoskeleton (Hoboken, N.J.) · 2025Article
- The cholesterol uptake regulator PCSK9 promotes and is a therapeutic target in APC/KRAS-mutant colorectal cancer.Nature communications · 2022Article
- A stop-gain mutation in GXYLT1 promotes metastasis of colorectal cancer via the MAPK pathway.Cell death & disease · 2022Article
- DIscBIO: A User-Friendly Pipeline for Biomarker Discovery in Single-Cell Transcriptomics.International journal of molecular sciences · 2021Article
- Structure-based discovery of small molecule APC-Asef interaction inhibitors: In silico approaches and molecular dynamics simulations.Journal of molecular modeling · 2020Article
- Design and Synthesis of TASIN Analogues Specifically Targeting Colorectal Cancer Cell Lines with Mutant Adenomatous Polyposis Coli (APC).Journal of medicinal chemistry · 2019Article
- Adenomatous Polyposis Coli (APC) in cell migration.European journal of cell biologyReview
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Adenomatous polyposis coli (APC) is a key molecule to maintain cellular homeostasis in colonic epithelium by regulating cell-cell adhesion, cell polarity, and cell migration through activating the APC-stimulated guanine nucleotide-exchange factor (Asef). The APC-activated Asef stimulates the small GTPase, which leads to decreased cell-cell adherence and cell polarity, and enhanced cell migration. In colorectal cancers, while truncated APC constitutively activates Asef and promotes cancer initiation and progression, regulation of Asef by full-length APC is still unclear. Here, we report the autoinhibition mechanism of full-length APC. We found that the armadillo repeats in full-length APC interact with the APC residues 1362 to 1540 (APC-2,3 repeats), and this interaction competes off and inhibits Asef. Deletion of APC-2,3 repeats permits Asef interactions leading to downstream signaling events, including the induction of Golgi fragmentation through the activation of the Asef-ROCK-MLC2. Truncated APC also disrupts protein trafficking and cholesterol homeostasis by inhibition of SREBP2 activity in a Golgi fragmentation-dependent manner. Our study thus uncovers the autoinhibition mechanism of full-length APC and a novel gain of function of truncated APC in regulating Golgi structure, as well as cholesterol homeostasis, which provides a potential target for pharmaceutical intervention against colon cancers.
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