Gene expression of <i>cyclin‐dependent kinase subunit Cks2</i> is repressed by the tumor suppressor p53 but not by the related proteins p63 or p73

Rother, Karen; Dengl, Markus; Lorenz, Jana; Tschöp, Katrin; Kirschner, R.; Mössner, Joachim; Engeland, Kurt

doi:10.1016/j.febslet.2007.02.028

Cited by 30 publications

(25 citation statements)

References 32 publications

(67 reference statements)

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“…Earlier studies identified CKS2 as a transcriptional target that was downregulated by the tumor suppressor p53 (12). Other studies demonstrated that expression of CKS1 and CKS2 were elevated in prostate cancer, while knockdown of CKS2 expression induced programmed cell death and inhibited tumorigenicity (13).…”

Section: Discussionmentioning

confidence: 99%

Detection of differentially expressed genes and association with clinicopathological features in laryngeal squamous cell carcinoma

Shen

Qian

et al. 2012

Oncology Letters

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Abstract. Head and neck cancer is a significant health problem worldwide. Early detection and prediction of prognosis will improve patient survival and quality of life. The aim of this study was to identify genes differentially expressed between laryngeal cancer and the corresponding normal tissues as potential biomarkers. A total of 36 patients with laryngeal squamous cell carcinoma were recruited. Four of these cases were randomly selected for cDNA microarray analysis of the entire genome. Using semi-quantitative RT-PCR and western blot analysis, the differential expression of genes and their protein products, respectively, between laryngeal cancer tissues and corresponding adjacent normal tissues was verified in the remaining 32 cases. The expression levels of these genes and proteins were investigated for associations with clinicopathological parameters taken from patient data. The cDNA microarray analysis identified 349 differentially expressed genes between tumor and normal tissues, 112 of which were upregulated and 237 were downregulated in tumors. Seven genes and their protein products were then selected for validation using RT-PCR and western blot analysis, respectively. The data demonstrated that the expression of SENP1, CD109, CKS2, LAMA3, ITGAV and ITGB8 was increased, while LAMA2 was downregulated in laryngeal cancer compared with the corresponding normal tissues. Associations between the expression of these genes and clinicopathological data from the patients were also established, including age, tumor classification, stage, differentiation and lymph node metastasis. Our current study provides the first evidence that these seven genes may be differentially expressed in laryngeal squamous cell carcinoma and also associated with clinicopathological data.Future study is required to further confirm whether detection of their expression can be used as biomarkers for prediction of patient survival or potential treatment targets. IntroductionHead and neck cancer is the sixth most common type of cancer in the world, accounting for more than 540,000 new cases and 271,000 mortalities each year (1). These cancers occur in the lips, oral cavity, nasal cavity, paranasal sinuses, pharynx and larynx, 90% of which are squamous cell carcinomas. They significantly affect long-term survival and the quality of life of patients. The development of novel strategies is required for prevention and early detection, to reduce cancer incidence and overcome problems associated with treatment of late-stage tumors. Improved prediction of outcome will lead to treatment decisions that prolong patients' survival and quality of life.Predictions concerning the outcome of head and neck cancers are currently based mostly on clinicopathological features, including tumor stage, differentiation, size and regional lymph node or distant metastasis. However, increasing numbers of studies utilize aberrant gene expression and genomic and epigenetic alterations to predict prognosis.It has been established that tobacco smoke and alcohol consump...

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Section: Discussionmentioning

confidence: 99%

Detection of differentially expressed genes and association with clinicopathological features in laryngeal squamous cell carcinoma

Shen

Qian

et al. 2012

Oncology Letters

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“…Cks2 is required for the first metaphase/anaphase transition of mammalian meiosis, and was also found to be upregulated in colon cancer metastases [33,34], prostate and gastric cancer [35,36], and hepatocellular carcinomas [37]. Recent data showed that gene expression of cyclin-dependent kinase subunit Cks2 is repressed by the tumor suppressor p53 [38]. Although p53 mutations are rare in meningiomas [39], several reports showed higher expression in atypical and anaplastic meningiomas [40,41] and in one set of data based on an analysis of 80 meningiomas, specifically in grade I relapsing meningiomas [42].…”

Section: Discussionmentioning

confidence: 99%

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

Menghi¹,

Orzan²,

Eoli³

et al. 2011

The Oncologist

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Meningiomas are the most frequent intracranial tumors. Surgery can be curative, but recurrences are possible. We performed gene expression analyses and loss of heterozygosity (LOH) studies looking for new markers predicting the recurrence risk. We analyzed expression profiles of 23 meningiomas (10 grade I, 10 grade II, and 3 grade III) and validated the data using quantitative polymerase chain reaction (qPCR). We performed LOH analysis on 40 meningiomas, investigating chromosomal regions on 1p, 9p, 10q, 14q, and 22q. We found 233 and 268 probe sets to be significantly down-and upregulated, respectively, in grade II or III meningiomas. Genes downregulated in high-grade meningiomas were overrepresented on chromosomes 1, 6, 9, 10, and 14. Based on functional enrichment analysis, we selected LIM domain and actin binding 1 (LIMA1), tissue inhibitor of metalloproteinases 3 (TIMP3), cyclin-dependent kinases regulatory subunit 2 (CKS2), leptin receptor (LEPR), and baculoviral inhibitor of apoptosis repeat-containing 5 (BIRC5) for validation using qPCR and confirmed their differential expression in the two groups of tumors. We calculated ⌬Ct values of CKS2 and LEPR and found that their differential expression (C-L index) was significantly higher in grade I than in grade II or III meningiomas (p < .0001). Interestingly, the C-L index of nine grade I meningiomas from patients who relapsed in <5 years was significantly lower than in grade I meningiomas from patients who did not relapse. These findings indicate that the C-L index may be relevant to define the progression risk in meningioma patients, helping guide their clinical management. A prospective analysis on a larger number of cases is warranted.

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“…Cancer Res 2007; 67: (21 (24,25), and CKS2 (26). Each of these targets is either directly or indirectly related to competency for cell cycle progression, indicating novel cell growth regulatory roles for the HiNF-P/p220…”

Section: Cancer Researchmentioning

confidence: 99%

The HiNF-P/p220NPAT Cell Cycle Signaling Pathway Controls Nonhistone Target Genes

et al. 2007

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HiNF-P and its cofactor p220NPAT are principal factors regulating histone gene expression at the G 1 -S phase cell cycle transition. Here, we have investigated whether HiNF-P controls other cell cycle-and cancer-related genes. We used cDNA microarrays to monitor responsiveness of gene expression to small interfering RNA-mediated depletion of HiNF-P. Candidate HiNF-P target genes were examined for the presence of HiNF-P recognition motifs, in vitro HiNF-P binding to DNA, and in vivo association by chromatin immunoprecipitations and functional reporter gene assays. Of 177 proliferation-related genes we tested, 20 are modulated in HiNF-P-depleted cells and contain putative HiNF-P binding motifs. We validated that at least three genes (i.e., ATM, PRKDC, and CKS2) are HiNF-P dependent and provide data indicating that the DNA damage response is altered in HiNF-P-depleted cells. We conclude that, in addition to histone genes, HiNF-P also regulates expression of nonhistone targets that influence competency for cell cycle progression. [Cancer Res 2007;67(21):10334-42]

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Gene expression of cyclin‐dependent kinase subunit Cks2 is repressed by the tumor suppressor p53 but not by the related proteins p63 or p73

Cited by 30 publications

References 32 publications

Detection of differentially expressed genes and association with clinicopathological features in laryngeal squamous cell carcinoma

Detection of differentially expressed genes and association with clinicopathological features in laryngeal squamous cell carcinoma

DNA Microarray Analysis Identifies CKS2 and LEPR as Potential Markers of Meningioma Recurrence

The HiNF-P/p220NPAT Cell Cycle Signaling Pathway Controls Nonhistone Target Genes

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