CCND3

CCND3

A gene on chromosome 6p21 that encodes a member of the highly conserved cyclin family, which regulates CDK kinases. Cyclin D3 forms a complex with and is a regulatory subunit of CDK4 or CDK6, which are required for cell cycle G1/S transition. It also interacts with tumour suppressor protein Rb and is involved in its phosphorylation. The cyclin D3-CDK4 complex is involved in cell cycle progression through G2 phase into mitosis after UV light-induced damage.
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Translocations targeting CCND2, CCND3, and MYCN do occur in t(11;14)-negative mantle cell lymphomas.
Here, we describe a suite of ddPCR assays for detecting and quantifying clinically relevant EZH2, STAT6, MYD88, and CCND3 mutations in B-cell lymphomas.
We designed Custom PrimeTime[R] Mini LNA probes and ZEN double-quenched hydrolysis probes (Integrated DNA Technologies) for EZH2 (Y641), STAT6 (D419), MYD88 (L265), and CCND3 (I290) hotspots, as described in the online Supplemental Methods file.
Based on target prediction programs (miRTarBase, TargetScan, miRanda, and MiRBase) and published papers, we found highly evidenced candidate target genes (hypoxia-inducible factor 1A and Cullin 2 genes for hypoxia and angiogenesis; cyclin-dependent kinase 6 (CDK6), Cyclin D1 (CCND1), Cyclin E1 (CCNE1), and CCND3 genes for cell cycle) of hsa-miR-424-5p.
Candidate target genes of hsa-miR-424-5p and hsa-miR-377 Gene name Main pathway Target Accession gene ID hsa-miR-424-5p Hypoxia and angiogenesis HIF1A MIRT005926 CUL2 MIRT005927 Cell cycle CDK6 MIRT000938 CCND1 MIRT000941 CCNE1 MIRT000936 CCND3 MIRT000937 hsa-miR-377 MAPK pathway PPM1A MIRT000990 PI3K-akt pathway PAK1 MIRT000991 HIF1A: Hypoxia-inducible factor 1A; CUL2: Cullin 2; CDK: Cyclin-dependent kinase; CCND1: Cyclin D1; CCNE1: Cyclin E1; CCND3: Cyclin D3; MAPK: Mitogen-activated protein kinase; PPM1A: Protein phosphatase magnesium-dependent 1A; PI3K: Phosphatidyl inositol 3'-kinase; PAK1: p21-activated kinase 1.
Researchers were able to demonstrate that the enzymatic activity of PFTK1 was dependent upon CCND3 and was negatively regulated by p21.
63) Carcinoma in situ has a high rate of TP53 mutations, (64) and the following genetic mutation rates have been reported for urothelial carcinoma: PIK3CA, 26%; CDKN2A/B, 23%; RB1, 17%; CCND1, 14%; FGFR1, 14%; CCND3, 11%; FGFR3, 11%; MDM2, 11%; EGFR, 6%; and HER2/neu, 6%.
The most-common, potentially targetable alterations were mutations, amplifications, and homozygous deletions of PIK3CA (n = 8; 40%), PTEN (n = 5; 25%), CDKN2A/B (n = 4; 20%), CCND3 (n = 3; 15%), CCNE1 (n = 2; 10%), and EGFR (n = 2; 10%), with AKT3, CCND1, CCND2, CDK4, FBXW7, FGFR1, HRAS, NF1, PIK3R1, and SRC altered in a single case (Figure 1; Table 1).
Cell-cycle alterations were common, including homozygous deletion of CDKN2A in 4 (20%) and amplifications of CCND3, CCNE1, CCND1, CCND2, and CDK4 in 8 (40%) of the MPBC cases, a subset of which may indicate the potential for use of cell-cycle inhibitors.
These rearrangements can involve more than a dozen partners, including CCND1-XT (chromosome 11), FGFR3 (chromosome 4), MAF (chromosome 16), CCND3 (chromosome 6), and MAFB (chromosome 20), as well as unknown partners.
In this case, the uIgH most likely resulted from, IgH rearrangement involving a non-high-risk partner, such as CCND3, (1,8,35) or others that were undetectable by the FISH probes used in this study.
They found CCND3 expression to be highly sensitive and specific for recurrence (97% and 63%, respectively).