ArticlePathology oncology research : POR2017
Systematic Investigation of Expression of G2/M Transition Genes Reveals CDC25 Alteration in Nonfunctioning Pituitary Adenomas.
Article in Pathology oncology research : POR, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 24 citations in OpenAlex.
- Identification and validation of susceptibility modules and hub genes of adrenocortical carcinoma through WGCNA and machine learning.Discover oncology · 2025Article
- Increased Prevalence of Germline Pathogenic CHEK2 Variants in Individuals With Pituitary Adenomas.The Journal of clinical endocrinology and metabolism · 2024Article
- Aspirin Mediates Its Antitumoral Effect Through Inhibiting PTTG1 in Pituitary Adenoma.The Journal of clinical endocrinology and metabolism · 2022Article
- Tat-NTS Suppresses the Proliferation, Migration and Invasion of Glioblastoma Cells by Inhibiting Annexin-A1 Nuclear Translocation.Cellular and molecular neurobiology · 2022Article
- Diagnostic value of abnormal chromosome 3p genes in small-cell lung cancer.Oncology letters · 2022Article
- Delayed Craniospinal Metastasis of Aggressive Nonfunctioning Pituitary Adenomas as Pituitary Carcinomas.Journal of neurological surgery. Part B, Skull base · 2022Article
- Muti-omics integration analysis revealed molecular network alterations in human nonfunctional pituitary neuroendocrine tumors in the framework of 3P medicine.The EPMA journal · 2022Review
- Review
- MiRNAs as Noninvasive Biomarkers and Therapeutic Agents of Pituitary Adenomas.International journal of molecular sciences · 2020Review
- The Search of miRNA Related to Invasive Growth of Nonfunctioning Gonadotropic Pituitary Tumors.International journal of endocrinology · 2020Article
- Limitations of high throughput methods for miRNA expression profiles in non-functioning pituitary adenomas.Pathology oncology research : POR · 2019Article
- Survivin as a potential therapeutic target of acetylsalicylic acid in pituitary adenomas.Oncotarget · 2018Article
- Comprehensive analysis of differential expression profiles reveals potential biomarkers associated with the cell cycle and regulated by p53 in human small cell lung cancer.Experimental and therapeutic medicine · 2018Article
- Advancements in the study of miRNA regulation during the cell cycle in human pituitary adenomas.Journal of neuro-oncology · 2017Review
- A focused evaluation of genetic and epigenetic contributions to common infertility conditions.Therapeutic advances in reproductive healthReview
- Article
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Authors and funding
12 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dysregulation of G1/S checkpoint of cell cycle has been reported in pituitary adenomas. In addition, our previous finding showing that deregulation of Wee1 kinase by microRNAs together with other studies demonstrating alteration of G2/M transition in nonfunctioning pituitary adenomas (NFPAs) suggest that G2/M transition may also be important in pituitary tumorigenesis. To systematically study the expression of members of the G2/M transition in NFPAs and to investigate potential microRNA (miRNA) involvement. Totally, 80 NFPA and 14 normal pituitary (NP) tissues were examined. Expression of 46 genes encoding members of the G2/M transition was profiled on 34 NFPA and 10 NP samples on TaqMan Low Density Array. Expression of CDC25A and two miRNAs targeting CDC25A were validated by individual quantitative real time PCR using TaqMan assays. Protein expression of CDC25A, CDC25C, CDK1 and phospho-CDK1 (Tyr-15) was investigated on tissue microarray and immunohistochemistry. Several genes' expression alteration were observed in NFPA compared to normal tissues by transcription profiling. On protein level CDC25A and both the total and the phospho-CDK1 were overexpressed in adenoma tissues. CDC25A correlated with nuclear localized CDK1 (nCDK1) and with tumor size and nCDK1 with Ki-67 index. Comparing primary vs. recurrent adenomas we found that Ki-67 proliferation index was higher and phospho-CDK1 (inactive form) was downregulated in recurrent tumors compared to primary adenomas. Investigating the potential causes behind CDC25A overexpression we could not find copy number variation at the coding region nor expression alteration of CDC25A regulating transcription factors however CDC25A targeting miRNAs were downregulated in NFPA and negatively correlated with CDC25A expression. Our results suggest that among alterations of G2/M transition of the cell cycle, overexpression of the CDK1 and CDC25A may have a role in the pathogenesis of the NFPA and that CDC25A is potentially regulated by miRNAs.
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