ReviewThe international journal of biochemistry & cell biology2017
Expression and alternative splicing of the cyclin-dependent kinase inhibitor-3 gene in human cancer.
Review in The international journal of biochemistry & cell biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- Integrating single-cell RNA sequencing, WGCNA, and machine learning to identify key biomarkers in hepatocellular carcinoma.Scientific reports · 2025Article
- The role of Cyclin Dependent Kinase Inhibitor 3 (Heliyon · 2024Review
- Article
- Identification and validation of functional roles for three MYC-associated genes in hepatocellular carcinoma.Journal of advanced research · 2023Article
- Comprehensive Analysis Reveals the Potential Roles of CDKN3 in Pancancer and Verification in Endometrial Cancer.International journal of general medicine · 2023Article
- A Novel Insight into Paraptosis-Related Classification and Signature in Lower-Grade Gliomas.International journal of genomics · 2022Article
- Survival-associated alternative splicing events interact with the immune microenvironment in stomach adenocarcinoma.World journal of gastroenterology · 2021Article
- KRT18 Modulates Alternative Splicing of Genes Involved in Proliferation and Apoptosis Processes in Both Gastric Cancer Cells and Clinical Samples.Frontiers in genetics · 2021Article
- Identification of hub genes associated with esophageal cancer progression using bioinformatics analysis.Oncology letters · 2020Article
- Transcriptome analysis of neratinib treated HER2 positive cancer model vs untreated cancer unravels the molecular mechanism of action of neratinib.Saudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2020Article
- CDKN3 expression predicates poor prognosis and regulates adriamycin sensitivity in hepatocellular carcinomaThe Journal of international medical research · 2020Article
- Integrated analysis of a compendium of RNA-Seq datasets for splicing factors.Scientific data · 2020Article
- CDKN3 promotes cell proliferation, invasion and migration by activating the AKT signaling pathway in esophageal squamous cell carcinoma.Oncology letters · 2020Article
- CDKN3 promotes tumor progression and confers cisplatin resistance via RAD51 in esophageal cancer.Cancer management and research · 2019Article
- Specification of Drosophila neuropeptidergic neurons by the splicing component brr2.PLoS genetics · 2018Article
- Article
- RBPMetaDB: a comprehensive annotation of mouse RNA-Seq datasets with perturbations of RNA-binding proteins.Database : the journal of biological databases and curation · 2018Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
The cyclin-dependent kinase inhibitor-3 (CDKN3) gene encodes a dual-specificity protein tyrosine phosphatase that dephosphorylates CDK1/CDK2 and other proteins. CDKN3 is often overexpressed in human cancer, and this overexpression correlates with reduced survival in several types of cancer. CDKN3 transcript variants and mutations have also been reported. The mechanism of CDKN3 overexpression and the role of CDKN3 transcript variants in human cancer are not entirely clear. Here, we review the literature and provide additional data to assess the correlation of CDKN3 expression with patient survival. Besides the full-length CDKN3 encoding transcript and a major transcript that skips exon 2 express in normal and cancer cells, minor aberrant transcript variants have been reported. Aberrant CDKN3 transcripts were postulated to encode dominant-negative inhibitors of CDKN3 as an explanation for overexpression of the perceived tumor suppressor gene in human cancer. However, while CDKN3 is often overexpressed in human cancer, aberrant CDKN3 transcripts occur infrequently and at lower levels. CDKN3 mutations and copy number alternation are rare in human cancer, implying that neither loss of CDKN3 activity nor constitutive gain of CDKN3 expression offer an advantage to tumorigenesis. Recently, it was found that CDKN3 transcript and protein levels fluctuate during the cell cycle, peaking in mitosis. Given that rapidly growing tumors have more mitotic cells, the high level of mitotic CDKN3 expression is the most plausible mechanism of frequent CDKN3 overexpression in human cancer. This finding clarifies the mechanism of CDKN3 overexpression in human cancer and questions the view of CDKN3 as a tumor suppressor.
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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.