The DOI matches its Crossref record; 105 of the 110 references it cites were found in a registry or an index.
PTENless means more
Open accessAbstract
Recent studies indicate that certain key molecules that are vital for various developmental processes, such as Wnt, Shh, and Notch, cause cancer when dysregulated. PTEN, a tumor suppressor that antagonizes the PI3 kinase pathway, is the newest one on the list. The biological function of PTEN is evolutionarily conserved from C. elegans to humans, and the PTEN-controlled signaling pathway regulates cellular processes crucial for normal development, including cell proliferation, soma growth, cell death, and cell migration. In this review, we will focus on the function of PTEN in murine development and its role in regulating stem cell self-renewal and proliferation. We will summarize the organomegaly phenotypes associated with Pten tissue-specific deletion and discuss how PTEN controls organ size, a fundamental aspect of development. Last, we will review the role of PTEN in hormone-dependent, adult-onset mammary and prostate gland development.
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“Furthermore, knockdown of PTEN in mammary epithelial cells grown in 3D culture results in hyperproliferation and disrupted acinar organization (37).”
From Mislocalization of the Cell Polarity Protein Scribble Promotes Mammary Tumorigenesis and Is Associated with Basal Breast Cancer (2014) · cites this paper as [37]
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Metadata
- Authors
- Stiles, B., Groszer, M., Wang, S., Jiao, J., & Wu, H.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Wu, Hong
- Venue
- Developmental Biology
- Publisher
- Elsevier BV
- Published
- 2004-09
- Volume
- 273
- Issue
- 2
- Pages
- 175-184
- ISSN
- 0012-1606 (ISSN-L)
- OpenAlex
- W2001800178
- Cited by
- 230
- References
- 110
- Citations by year
- 2025: 1 · 2024: 5 · 2023: 5 · 2022: 2 · 2021: 11 · 2020: 8 · 2019: 4 · 2018: 2 · 2017: 4 · 2016: 6 · 2015: 12 · 2014: 9 · 2013: 13 · 2012: 8
- FWCI
- 1.50
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Developmental Biology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Howard Hughes Medical Institute
- National Cancer Institute (CA-98-013)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › PI3K/AKT/mTOR signaling in cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Developmental Biology and Gene Regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Hippo pathway signaling and YAP/TAZ
- Keywords
- PTEN, tumor suppressor, PI3 kinase pathway, organomegaly, organ size control, stem cell self-renewal, cell proliferation, mammary gland development, developmental signaling, Wnt, Sonic hedgehog, notches
- MeSH terms
- Animals, Cell Movement, Female, Embryonic and Fetal Development, Hormones, Humans, Male, Models, Biological, Stem Cells, Signal Transduction, Protein Tyrosine Phosphatases, Gene Expression Regulation, Developmental, Tumor Suppressor Proteins, PTEN Phosphohydrolase, Mice
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