G1/S-Specific Cyclin-E2

2020 ◽  
Author(s):  
Keyword(s):  
Cyclin E2

scholarly journals Cdc6 and Cyclin E2 Are PTEN-Regulated Genes Associated with Human Prostate Cancer Metastasis

Neoplasia ◽  
2009 ◽  
Vol 11 (1) ◽  
pp. 66-76 ◽  
Author(s):  
Zhong Wu ◽  
HyungJun Cho ◽  
Garret M. Hampton ◽  
Dan Theodorescu
Keyword(s):  
Prostate Cancer ◽  
Cancer Metastasis ◽  
Human Prostate ◽  
Human Prostate Cancer ◽  
Cyclin E2 ◽  
Prostate Cancer Metastasis

scholarly journals miR-3687 Overexpression Promotes Bladder Cancer Cell Growth by Inhibiting the Negative Effect of FOXP1 on Cyclin E2 Transcription

2019 ◽  
Vol 27 (5) ◽  
pp. 1028-1038
Author(s):  
Qipeng Xie ◽  
Caiyi Chen ◽  
Haiying Li ◽  
Jiheng Xu ◽  
Lei Wu ◽  
...  
Keyword(s):  
Bladder Cancer ◽  
Cell Growth ◽  
Cancer Cell ◽  
Bladder Cancer Cell ◽  
Cancer Cell Growth ◽  
Cyclin E2 ◽  
Negative Effect

Invariant Deletion of One Mir-34b/C Locus in CLL with del11q.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2074-2074
Author(s):  
Sami Malek ◽  
Peter Ouillette
Keyword(s):  
Target Genes ◽  
Snp Array ◽  
Response Duration ◽  
Selective Advantage ◽  
Clinical Syndrome ◽  
Expression Levels ◽  
Microrna Gene ◽  
Cyclin E2 ◽  
Potential Contributor ◽  
P53 Target Genes

Abstract CLL with del11q constitutes a clinical syndrome characterized by a relatively aggressive disease course, short response duration to therapies and compromised overall survival. CLL with del11q carries mutations in ATM in about one third of cases, which may further negatively affect prognosis. Little is known about additional molecular changes within or due to del11q in CLL and it remains unclear what the selective advantage of acquisition of del11q is for CLL cells. To gain insights into the physiology of CLL with del11q, we have mapped this lesion using the Affymetrix 50K SNP array platform in 178 CLL cases using DNA from sorted CD19+ cells versus paired buccal DNA. Focusing on the region that spans ATM, a minimal deleted region (MDR) of approximately 8 Mb was identified, spanning approximately 106.6–114.6 Mb physical position. Scanning the MDR for genes with the potential to affect the physiology of cancerous cells uncovered invariant monoallelic deletion of the miR-34b/c gene, the only known human microRNA gene within the del11q MDR. miR-34a-c have been implicated as direct p53 target genes by a number of groups and these microRNAs have been shown to be direct regulators of pro-proliferative and anti-apoptotic genes, including E2F3, Cyclin E2, Cdk6 and Bcl2. Given that ATM acts upstream of p53 in the ds-DNA damage response pathway, it appears that del11q lesions in CLL affect p53 apoptotic effector functions through two independent processes (ATM loss or mutation and miR-34b/c loss). Work is in progress measuring miR-34 b/c expression levels in a large CLL cohort and correlating miR-34b/c levels with expression levels of critical miR-34 targets in CLL. In summary, our data implicate miR-34b/c loss as a potential contributor to the physiology of del11q in CLL and should stimulate investigations into miR-34 function as a response predictor of therapy for CLL.

scholarly journals Cyclin E2, a Novel G1 Cyclin That Binds Cdk2 and Is Aberrantly Expressed in Human Cancers

1999 ◽  
Vol 19 (1) ◽  
pp. 612-622 ◽  
Author(s):  
Jean M. Gudas ◽  
Marc Payton ◽  
Sushil Thukral ◽  
Eddy Chen ◽  
Michael Bass ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Mammalian Cells ◽  
Cell Cycle Progression ◽  
Expressed Sequence Tag ◽  
Cyclin E ◽  
Cyclin E1 ◽  
Acid Protein ◽  
Cyclin E2 ◽  
Rate Limiting ◽  
Amino Acid Protein

ABSTRACT A novel cyclin gene was discovered by searching an expressed sequence tag database with a cyclin box profile. The human cyclin E2 gene encodes a 404-amino-acid protein that is most closely related to cyclin E. Cyclin E2 associates with Cdk2 in a functional kinase complex that is inhibited by both p27Kip1 and p21Cip1. The catalytic activity associated with cyclin E2 complexes is cell cycle regulated and peaks at the G1/S transition. Overexpression of cyclin E2 in mammalian cells accelerates G1, demonstrating that cyclin E2 may be rate limiting for G1 progression. Unlike cyclin E1, which is expressed in most proliferating normal and tumor cells, cyclin E2 levels were low to undetectable in nontransformed cells and increased significantly in tumor-derived cells. The discovery of a novel second cyclin E family member suggests that multiple unique cyclin E-CDK complexes regulate cell cycle progression.

scholarly journals Cyclin E2 is the predominant E-cyclin associated with NPAT in breast cancer cells

Cell Division ◽  
2015 ◽  
Vol 10 (1) ◽  
Author(s):  
Samuel Rogers ◽  
Brian S Gloss ◽  
Christine S Lee ◽  
Claudio Marcelo Sergio ◽  
Marcel E Dinger ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Cancer Cells ◽  
Breast Cancer Cells ◽  
Cyclin E2

Cyclin D1 and cyclin E2 are differentially expressed in gastric cancer

2016 ◽  
Vol 33 (5) ◽  
Author(s):  
Soni Kumari ◽  
Puneet ◽  
Shyam Babu Prasad ◽  
Suresh Singh Yadav ◽  
Mohan Kumar ◽  
...  
Keyword(s):  
Gastric Cancer ◽  
Cyclin D1 ◽  
Differentially Expressed ◽  
Cyclin E2

scholarly journals Cyclin B3 is dispensable for mouse spermatogenesis

2019 ◽  
Author(s):  
Mehmet E. Karasu ◽  
Scott Keeney
Keyword(s):  
Homologous Chromosome ◽  
Histological Analysis ◽  
Seminiferous Tubules ◽  
Specific Expression ◽  
Cyclin Dependent Kinases ◽  
Meiotic Progression ◽  
Chromosome Synapsis ◽  
Cyclin E2 ◽  
Sexual Production ◽  
Cyclin B3

AbstractCyclins, as regulatory partners of cyclin-dependent kinases (CDKs), control the switch-like cell cycle transitions that orchestrate orderly duplication and segregation of genomes. Compared to mitosis, relatively little is known about how cyclin-CDK complexes control meiosis, the specialized cell division that generates gametes for sexual production. Mouse cyclin B3 was previously shown to have expression restricted to the beginning of meiosis, making it a candidate to regulate meiotic events. Indeed, female mice lacking cyclin B3 are sterile because oocytes arrest at the metaphase-to-anaphase transition of meiosis I. However, whether cyclin B3 functions during spermatogenesis was untested. Here, we found that males lacking cyclin B3 are fertile and show no detectable defects in spermatogenesis based on histological analysis of seminiferous tubules. Cytological analysis further showed no detectable defects in homologous chromosome synapsis or meiotic progression, and suggested that recombination is initiated and completed efficiently. Moreover, absence of cyclin B3 did not exacerbate previously described meiotic defects in mutants deficient for cyclin E2, suggesting a lack of redundancy between these cyclins. Thus, unlike in females, cyclin B3 is not essential for meiosis in males despite its prominent meiosis-specific expression.

miR-29b Derived from Bone Marrow Stromal Cell (BMSC) Exosomes Improves Laryngeal Carcinoma by Inhibiting Forkhead Box Protein P1 (FOXP1) to Decrease Cyclin E2 Transcription

2022 ◽  
Vol 12 (3) ◽  
pp. 617-624
Author(s):  
Juan Zheng ◽  
Liang Zhou
Keyword(s):  
Cell Cycle ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Laryngeal Cancer ◽  
Soft Agar ◽  
Cell Cycle Distribution ◽  
Soft Agar Assay ◽  
Cyclin E2 ◽  
Targeted Inhibition

This study intends to investigate whether miR-29b derived from BMSC exosomes (BMSC-exos) affects laryngeal cancer progression. RT-qPCR detected miR-29b level in BMSCs and BMSC-exos. After miR-29b was overexpressed in BMSCs, exos were extracted from BMSCs and used to treat laryngeal cancer cells, followed by CCK-8 assay and soft agar assay. When cells were treated with FOXP1 inhibitor or cyclin E2 vector, Western blot analyzed the expression of related proteins and flow cytometry assessed cell cycle distribution. In vivo experiment was conducted to assess miR-29b’s effect on tumor growth. miR-29b was upregulated in BMSC-exos, but lowly expressed in cancer cells. miR-29b upregulation inhibited the proliferation of laryngeal cancer cells and delayed tumor progression In vivo by inducing cell cycle arrest. Importantly, miR-29b bound 3′UTR of FXOP1 to inhibit its expression, and further reduced cyclin E2 level. sh-FXOP1 or cyclin E2 vector can restore the cell cycle and proliferation caused by miR-29b. In conclusion, miR-29b enriched in BMSC-exo can down-regulate cyclin E2 expression through targeted inhibition of FXOP1, thereby inhibiting the progression of laryngeal cancer.

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