ReviewExperimental & molecular medicine2009
The function of p27 KIP1 during tumor development.
Review in Experimental & molecular medicine, 2009. 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, 109 citations in OpenAlex.
- Adipogenesis Under Leptin Control: Mechanisms and Model-Specific Effects.International journal of molecular sciences · 2026Review
- Genetic variants linked to type 2 diabetes in CDKN1B and TCF7L2 influence survival outcomes in metastatic colorectal cancer.International journal of cancer · 2025Article
- SENP1 promotes p27kip1 nuclear export though enhanced SUMOylation in cholangiocarcinoma leading to increased cell proliferation and chemoresistance.International journal of molecular medicine · 2025Article
- HES1 in cancer: a key player in tumorigenesis and its prognostic significance.Molecular genetics and genomics : MGG · 2025Review
- Impact of G1 phase kinetics on the acquisition of stemness in cancer cells: the critical role of cyclin D.Molecular biology reports · 2025Review
- The Homeobox Transcription Factor NKX3.1 Displays an Oncogenic Role in Castration-Resistant Prostate Cancer Cells.Cancers · 2025Article
- ACKnowledging the role of the Activated-Cdc42 associated kinase (ACK) in regulating protein stability in cancer.Small GTPases · 2023Review
- Canonical Wnt and TGF-β/BMP signaling enhance melanocyte regeneration but suppress invasiveness, migration, and proliferation of melanoma cells.Frontiers in cell and developmental biology · 2023Article
- R-PTP-κ Inhibits Contact-Dependent Cell Growth by Suppressing E2F Activity.Biomedicines · 2022Article
- Construing the metaxin-2 mediated simultaneous localization between mitochondria and nucleolus using molecular viscometry.Chemical science · 2022Article
- Induction of p27 contributes to inhibitory effect of isorhapontigenin (ISO) on malignant transformation of human urothelial cells.Cell cycle (Georgetown, Tex.) · 2022Article
- Decomposition of cell activities revealing the role of the cell cycle in driving biofunctional heterogeneity.Scientific reports · 2021Article
- The role of HPV-induced epigenetic changes in cervical carcinogenesis (Review).Biomedical reports · 2021Review
- The Role of Immunohistochemical Markers for the Diagnosis and Prognosis of Adrenocortical Neoplasms.Journal of personalized medicine · 2021Article
- The long non-coding RNA landscape in triple-negative breast cancer.Cell proliferation · 2021Review
- CD155 Promotes the Progression of Cervical Cancer Cells Through AKT/mTOR and NF-κB Pathways.Frontiers in oncology · 2021Article
- Increased Expression of NPM1 Suppresses p27Cancers · 2020Article
- RABL6A Is an Essential Driver of MPNSTs that Negatively Regulates the RB1 Pathway and Sensitizes Tumor Cells to CDK4/6 Inhibitors.Clinical cancer research : an official journal of the American Association for Cancer Research · 2020Article
- Common Functions of Disordered Proteins across Evolutionary Distant Organisms.International journal of molecular sciences · 2020Review
- Synemin Redefined: Multiple Binding Partners Results in Multifunctionality.Frontiers in cell and developmental biology · 2020Review
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
2 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Timely cell cycle regulation is conducted by sequential activation of a family of serine-threonine kinases called cycle dependent kinases (CDKs). Tight CDK regulation involves cyclin dependent kinase inhibitors (CKIs) which ensure the correct timing of CDK activation in different phases of the cell cycle. One CKI of importance is p27(KIP1). The regulation and cellular localization of p27(KIP1) can result in biologically contradicting roles when found in the nucleus or cytoplasm of both normal and tumor cells. The p27(KIP1) protein is mainly regulated by proteasomal degradation and its downregulation is often correlated with poor prognosis in several types of human cancers. The protein can also be functionally inactivated by cytoplasmic localization or by phosphorylation. The p27(KIP1) protein is an unconventional tumor suppressor because mutation of its gene is extremely rare in tumors, implying the normal function of the protein is deranged during tumor development. While the tumor suppressor function is mediated by p27(KIP1)s inhibitory interactions with the cyclin/CDK complexes, its oncogenic function is cyclin/CDK independent, and in many cases correlates with cytoplasmic localization. Here we review the basic features and novel aspects of the p27(KIP1) protein, which displays genetically separable tumor suppressing and oncogenic functions.
Indexed as
Identifiers
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.