ReviewOncogene2008
Par complex in cancer: a regulator of normal cell polarity joins the dark side.
Review in Oncogene, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
64 citing papers in PubMed, 103 citations in OpenAlex.
- Porcine epidemic diarrhea virus influences the expression of tight junction proteins through the polarity protein PAR6.Virus genes · 2026Article
- Polarity protein Par3 deficiency promotes metastasis of bladder cancer via interaction of Ppp1r12c.Biology direct · 2026Article
- Par6/SOX2 interact to modulate stemness maintenance in glioma by regulating the EGFR/PI3K/AKT signaling cascade.Oncogene · 2025Article
- Phosphorylation by Aurora kinase A facilitates cortical-cytoplasmic dynamics of Par-3 in asymmetric division of radial glia progenitors.Science advances · 2025Article
- Cell polarity proteins promote macropinocytosis in response to metabolic stress.Nature communications · 2024Article
- Microenvironment-optimized gastrodin-functionalized scaffolds orchestrate asymmetric division of recruited stem cells in endogenous bone regeneration.Journal of nanobiotechnology · 2024Article
- PARD3 drives tumorigenesis through activating Sonic Hedgehog signalling in tumour-initiating cells in liver cancer.Journal of experimental & clinical cancer research : CR · 2024Article
- Hypoxia disrupt tight junctions and promote metastasis of oral squamous cell carcinoma via loss of par3.Cancer cell international · 2023Article
- Impact of peptide permeation enhancer on tight junctions opening cellular mechanisms.Biochemistry and biophysics reports · 2022Article
- Dissecting cell fate dynamics in pediatric glioblastoma through the lens of complex systems and cellular cybernetics.Biological cybernetics · 2022Review
- MicroRNAs as the critical regulators of cell migration and invasion in thyroid cancer.Biomarker research · 2022Review
- Partitioning defective 6 homolog alpha (PARD6A) promotes epithelial-mesenchymal transition via integrin β1-ILK-SNAIL1 pathway in ovarian cancer.Cell death & disease · 2022Article
- Polarity protein Par3 sensitizes breast cancer to paclitaxel by promoting cell cycle arrest.Breast cancer research and treatment · 2022Article
- Dual Function of Par3 in Tumorigenesis.Frontiers in oncology · 2022Review
- Role of RhoC in cancer cell migration.Cancer cell international · 2021Review
- Polarized endosome dynamics engage cytoplasmic Par-3 that recruits dynein during asymmetric cell division.Science advances · 2021Article
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- Emerging Themes in PDZ Domain Signaling: Structure, Function, and Inhibition.International review of cell and molecular biology · 2019Review
- aPKC controls endothelial growth by modulating c-Myc via FoxO1 DNA-binding ability.Nature communications · 2018Article
4 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
In the past 20 years, the discovery and characterization of the molecular machinery that controls cellular polarization have enabled us to achieve a better understanding of many biological processes. Spatial asymmetry or establishment of cell polarity during embryogenesis, epithelial morphogenesis, neuronal differentiation, and migration of fibroblasts and T cells are thought to rely on a small number of evolutionarily conserved proteins and pathways. Correct polarization is crucial for normal cell physiology and tissue homeostasis, and is lost in cancer. Thus, cell polarity signaling is likely to have an important function in tumor progression. Recent findings have identified a regulator of cell polarity, the Par complex, as an important signaling node in tumorigenesis. In normal cell types, the Par complex is part of the molecular machinery that regulates cell polarity and maintains normal cell homeostasis. As such, the polarity regulators are proposed to have a tumor suppressor function, consistent with the loss of polarity genes associated with hyperproliferation in Drosophila melanogaster. However, recent studies showing that some members of this complex also display pro-oncogenic activities suggest a more complex regulation of the polarity machinery during cellular transformation. Here, we examine the existing data about the different functions of the Par complex. We discuss how spatial restriction, binding partners and substrate specificity determine the signaling properties of Par complex proteins. A better understanding of these processes will very likely shed some light on how the Par complex can switch from a normal polarity regulation function to promotion of transformation downstream of oncogenes.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.