ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2016
The potential role of the NEK6, AURKA, AURKB, and PAK1 genes in adenomatous colorectal polyps and colorectal adenocarcinoma.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 34 citations in OpenAlex.
- Cellular reprogramming and signaling control by kaempferol in colorectal cancer.Discover oncology · 2026Review
- Dysregulation of Aurora Kinases andCurrent issues in molecular biology · 2026Article
- Fisetin Suppresses the Proliferative and Migratory Behavior of HeLa Cells by Modulating Aberrant Epigenetic Marks (Writers and Erasers).Epigenomes · 2026Article
- Kaempferol Targets Global Epigenetic Modifiers to Impedes Growth and Migratory Ability of HeLa Cells.Journal of cellular and molecular medicine · 2025Article
- Targeting NEK Kinases in Gastrointestinal Cancers: Insights into Gene Expression, Function, and Inhibitors.International journal of molecular sciences · 2025Review
- The NIMA-related kinase family and cancer.Frontiers in oncology · 2025Review
- Overexpression of Aurora Kinase B Is Correlated with Diagnosis and Poor Prognosis in Hepatocellular Carcinoma.International journal of molecular sciences · 2024Article
- Development and validation of epigenetic modification-related signals for the diagnosis and prognosis of colorectal cancer.BMC genomics · 2024Article
- NIMA-related kinase 6 as an effective target inhibits the hepatocarcinogenesis and progression of hepatocellular carcinoma.Heliyon · 2023Article
- Bioinformatics screening of colorectal-cancer causing molecular signatures through gene expression profiles to discover therapeutic targets and candidate agents.BMC medical genomics · 2023Article
- Exploring the components and mechanism ofFrontiers in oncology · 2023Article
- In Mitosis You Are Not: The NIMA Family of Kinases inInternational journal of molecular sciences · 2022Review
- Checking NEKs: Overcoming a Bottleneck in Human Diseases.Molecules (Basel, Switzerland) · 2020Review
- Control of clathrin-mediated endocytosis by NIMA family kinases.PLoS genetics · 2020Article
- Expression of the NEK family in normal and cancer tissue: an immunohistochemical study.BMC cancer · 2020Article
- Expression profiles of histone modification genes in gastric cancer progression.Molecular biology reports · 2018Article
- Circulating cell-free nucleosomes as biomarkers for early detection of colorectal cancer.Oncotarget · 2018Article
- Ubiquitination and regulation of AURKA identifies a hypoxia-independent E3 ligase activity of VHL.Oncogene · 2017Article
- Transcriptional landscape of human cancers.Oncotarget · 2017Article
- Identification of differentially expressed genes in the development of osteosarcoma using RNA-seq.Oncotarget · 2016Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Colorectal adenomatous polyp (CRAP) is a major risk factor for the development of sporadic colorectal cancer (CRC). Histone modifications are one of the epigenetic mechanisms that may have key roles in the carcinogenesis of CRC. The objective of the present study is to investigate the alternations in the defined histone modification gene expression profiles in patients with CRAP and CRC. Histone modification enzyme key gene expressions of the CRC, CRAP, and control groups were evaluated and compared using the reverse transcription PCR (RT-PCR) array method. Gene expression analysis was performed in the CRAP group after dividing the patients into subgroups according to the polyp diameter, pathological results, and morphological parameters which are risk factors for developing CRC in patients with CRAP. PAK1, NEK6, AURKA, AURKB, HDAC1, and HDAC7 were significantly more overexpressed in CRC subjects compared to the controls (p < 0.05). PAK1, NEK6, AURKA, AURKB, and HDAC1 were significantly more overexpressed in the CRAP group compared to the controls (p < 0.005). There were no significant differences between the CRAP and CRC groups with regards to PAK1, NEK6, AURKA, or AURKB gene overexpression. PAK1, NEK6, AURKA, and AURKB were significantly in correlation with the polyp diameter as they were more overexpressed in polyps with larger diameters. In conclusion, overexpressions of NEK6, AURKA, AURKB, and PAK1 genes can be used as predictive markers to decide the colonoscopic surveillance intervals after the polypectomy procedure especially in polyps with larger diameters.
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