The double dealing of cyclin D1

Abstract

Abbreviations: aa, amino acid ; AR, androgen receptor; ATM, ataxia telangectasia mutant;ATR, ATM and Rad3-related; CDK, cyclin-dependent kinase; ChREBP, carbohydrate response element binding protein; CIP, CDK-interacting protein; CHK1/2, checkpoint kinase 1/2; CKI, CDK inhibitor; DDR, DNA damage response; DMP1, cyclin D-binding myb-like protein; DSB, double-strand DNA break; DNA-PK, DNA-dependent protein kinase; ER, estrogen receptor; FASN, fatty acid synthase; GSK3β, glycogen synthase-3β; HAT, histone acetyltransferase; HDAC, histone deacetylase; HK2, hexokinase 2; HNF4α, and hepatocyte nuclear factor 4α; HR, homologous recombination; IR, ionizing radiation; KIP, kinase inhibitory protein; MCL, mantle cell lymphoma; NHEJ, non-homologous end-joining; PCAF, p300/CREB binding-associated protein; PGC1α, PPARγ co-activator 1α; PEST, proline-glutamic acid-serine-threonine, PK, pyruvate kinase; PPAR, peroxisome proliferator-activated receptor; RB1, retinoblastoma protein; ROS, reactive oxygen species; SRC, steroid receptor coactivator; STAT, signal transducer and activator of transcription; TGFβ, transforming growth factor β; UPS, ubiquitinproteasome system; USP22, ubiquitin-specific peptidase 22; XPO1 (or CRM1) exportin 1. AbstractThe cell cycle is tightly regulated by cyclins and their catalytic moieties, the cyclindependent kinases (CDKs). Cyclin D1, in association with CDK4/6, acts as a mitogenic sensor and integrates extracellular mitogenic signals and cell cycle progression. When deregulated (overexpressed, accumulated, inappropriately located), cyclin D1 becomes an oncogene and is recognized as a driver of solid tumors and hemopathies. Recent studies on the oncogenic roles of cyclin D1 reported non-canonical functions dependent on the partners of cyclin D1 and its location within tumor cells or tissues. Support for these new functions was provided by various mouse models of oncogenesis. Finally, proteomic and transcriptomic data identified complex cyclin D1 networks. This review focuses on these aspects of cyclin D1 pathophysiology, which may be crucial for targeted therapy.

Review: Local Tumor Necrosis Factor-α Inhibition in Inflammatory Bowel Disease

“…Additionally, the same research group [ 144 ] has investigated NiMOS containing a combination of siRNA against cyclin D1 (CyD1) and TNF-α (NiMOS-siRNA-CyD1). CyD1 is a protein involved in cell proliferation [ 161 ] and is overexpressed in IBD [ 162 , 163 ]. Similar effects with regards to TNF-α, cytokines, chemokines, histopathology and clinical improvements were observed whether the formulation contained siRNA against only TNF-α or CyD1—or a combination thereof given as a 1.2-mg/kg oral dose.…”

miR-20b-5p functions as tumor suppressor microRNA by targeting cyclinD1 in colon cancer

“…CCND1 is an important regulator of the G0/G1 transition in the cell cycle, and is often abnormally expressed in cancer and is a biomarker for cancer phenotype and disease progression [38] . CCND1 is an established human oncogene that is commonly overexpressed in tumor tissues, especially in lung cancer, melanoma and oral squamous cell carcinoma [32] .…”

Knockout of the Transducin-Like Enhancer of Split 6 Gene Affects the Proliferation and Cell Cycle Process of Mouse Spermatogonia

“…The transmission of restriction points is coordinated by two cyclin families, namely the cyclin D family and the cyclin E family. The activation sequence is that the D-type cyclin binds and activates cdk 4 and 6, and then cyclin E activates cdk2 [11,12]. Cyclin E targets the components of the DNA synthesis machinery, leading to the assembly of the complexes required for DNA replication [29].…”

“…In the advancement of the cell cycle, cyclin and CDK form a cyclin-CDK complex that affects cell proliferation. Researchers have indicated that the cyclin D-CDK 4 complex controls cells in the G0/G1 phase, while the cyclin E-CDK 2 complex controls cells from the G0/G1 phase to the S phase [12]. In the current research, the role of Tle6 on spermatogonia cell proliferation and the cell cycle was investigated using an immortalized mouse spermatogonia cell line, C18-4.…”