ArticleNeoplasia (New York, N.Y.)2013
PTEN phosphatase-independent maintenance of glandular morphology in a predictive colorectal cancer model system.
Article in Neoplasia (New York, N.Y.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 54 citations in OpenAlex.
- IRSp53 controls plasma membrane shape and polarized transport at the nascent lumen in epithelial tubules.Nature communications · 2020Article
- Disparate cell proliferation and p53 overexpression in colonic crypts with normal epithelial lining found below the neoplastic canopy of conventional adenomas.The journal of pathology. Clinical research · 2019Article
- New Routes in GPCR/β-Arrestin-Driven Signaling in Cancer Progression and Metastasis.Frontiers in pharmacology · 2019Review
- Mechanistic Insights into Colorectal Cancer Phenomics from Fundamental and Organotypic Model Studies.The American journal of pathology · 2018Review
- Protein kinase C zeta suppresses low- or high-grade colorectal cancer (CRC) phenotypes by interphase centrosome anchoring.The Journal of pathology · 2018Article
- PTEN controls glandular morphogenesis through a juxtamembrane β-Arrestin1/ARHGAP21 scaffolding complex.eLife · 2017Article
- Vitamin D3 suppresses morphological evolution of the cribriform cancerous phenotype.Oncotarget · 2016Article
- Antisense oligonucleotides against microRNA-21 reduced the proliferation and migration of human colon carcinoma cells.Cancer cell international · 2015Article
- Need for multi-scale systems to identify spindle orientation regulators relevant to tissue disorganization in solid cancers.Frontiers in physiology · 2014Article
- Cancer subclonal genetic architecture as a key to personalized medicine.Neoplasia (New York, N.Y.) · 2013Article
- Preliminary Report: Asymmetric Crypt Fission in Biopsies from Patients With Ulcerative Colitis.In vivo (Athens, Greece)Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Organotypic models may provide mechanistic insight into colorectal cancer (CRC) morphology. Three-dimensional (3D) colorectal gland formation is regulated by phosphatase and tensin homologue deleted on chromosome 10 (PTEN) coupling of cell division cycle 42 (cdc42) to atypical protein kinase C (aPKC). This study investigated PTEN phosphatase-dependent and phosphatase-independent morphogenic functions in 3D models and assessed translational relevance in human studies. Isogenic PTEN-expressing or PTEN-deficient 3D colorectal cultures were used. In translational studies, apical aPKC activity readout was assessed against apical membrane (AM) orientation and gland morphology in 3D models and human CRC. We found that catalytically active or inactive PTEN constructs containing an intact C2 domain enhanced cdc42 activity, whereas mutants of the C2 domain calcium binding region 3 membrane-binding loop (M-CBR3) were ineffective. The isolated PTEN C2 domain (C2) accumulated in membrane fractions, but C2 M-CBR3 remained in cytosol. Transfection of C2 but not C2 M-CBR3 rescued defective AM orientation and 3D morphogenesis of PTEN-deficient Caco-2 cultures. The signal intensity of apical phospho-aPKC correlated with that of Na(+)/H(+) exchanger regulatory factor-1 (NHERF-1) in the 3D model. Apical NHERF-1 intensity thus provided readout of apical aPKC activity and associated with glandular morphology in the model system and human colon. Low apical NHERF-1 intensity in CRC associated with disruption of glandular architecture, high cancer grade, and metastatic dissemination. We conclude that the membrane-binding function of the catalytically inert PTEN C2 domain influences cdc42/aPKC-dependent AM dynamics and gland formation in a highly relevant 3D CRC morphogenesis model system.
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