Cyclin-Dependent Kinases (CDK) and Their Role in Diseases Development–Review

Łukasik, Piotr; Załuski, Maciej; Gutowska, Izabela

doi:10.3390/ijms22062935

Cited by 36 publications

(30 citation statements)

References 333 publications

(198 reference statements)

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“…Targeting various pathways has become a major focus for an anticancer chemotherapeutic agent such as DNA damage-induced cell cycle arrest, DNA damage checkpoint kinases including CHK1/2 (checkpoint kinase 1/2), ATR (ataxia telangiectasia and rad3-related protein), and ATM (ataxia telangiectasia mutated) [ 69 , 70 , 71 , 72 , 73 ].…”

Section: Targets Of Tnbc Under Active Clinical Evaluationmentioning

confidence: 99%

TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy

Singh

Yadav

2021

Biomedicines

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Triple-negative breast cancer (TNBC) is a heterogeneous, recurring cancer associated with a high rate of metastasis, poor prognosis, and lack of therapeutic targets. Although target-based therapeutic options are approved for other cancers, only limited therapeutic options are available for TNBC. Cell signaling and receptor-specific targets are reportedly effective in patients with TNBC under specific clinical conditions. However, most of these cancers are unresponsive, and there is a requirement for more effective treatment modalities. Further, there is a lack of effective biomarkers that can distinguish TNBC from other BC subtypes. ER, PR, and HER2 help identify TNBC and are widely used to identify patients who are most likely to respond to diverse therapeutic strategies. In this review, we discuss the possible treatment options for TNBC based on its inherent subtype receptors and pathways, such as p53 signaling, AKT signaling, cell cycle regulation, DNA damage, and programmed cell death, which play essential roles at multiple stages of TNBC development. We focus on poly-ADP ribose polymerase 1, androgen receptor, vascular endothelial growth factor receptor, and epidermal growth factor receptor as well as the application of nanomedicine and immunotherapy in TNBC and discuss their potential applications in drug development for TNBC.

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“…Protein kinases are the most well studied category of mitotic factors that have been identified to play crucial roles in regulating mitochondrial dynamics, inheritance and function in mammalian cells. Among them, a lot of research has focused on the cyclin dependent kinase 1 CDK1-Cyclin B1 complex or maturation promoting factor (MPF), a major cell division kinase which controls the transition from G2 phase into mitosis ( Łukasik et al, 2021 ). Interestingly, an enzymatically active subfraction of CDK1-Cyclin B1 can be localized at mitochondria during G2/M phase, acting as a coordinator of mitochondrial bioenergetics to meet the high energy demand required to fuel this cell cycle transition ( Wang et al, 2014 ).…”

Section: How Does the Mitotic Machinery Regulate Mitochondrial Homeostasis?mentioning

confidence: 99%

The Multifaceted Regulation of Mitochondrial Dynamics During Mitosis

Pangou

Sumara²

2021

Front. Cell Dev. Biol.

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Mitosis ensures genome integrity by mediating precise segregation of the duplicated genetic material. Segregation of subcellular organelles during mitosis also needs to be tightly coordinated in order to warrant their proper inheritance and cellular homeostasis. The inheritance of mitochondria, a powerhouse of the cell, is tightly regulated in order to meet the high energy demand to fuel the mitotic machinery. Mitochondria are highly dynamic organelles, which undergo events of fission, fusion and transport during different cell cycle stages. Importantly, during mitosis several kinases phosphorylate the key mitochondrial factors and drive fragmentation of mitochondria to allow for their efficient distribution and inheritance to two daughter cells. Recent evidence suggests that mitochondrial fission can also actively contribute to the regulation of mitotic progression. This review aims at summarizing established and emerging concepts about the complex regulatory networks which couple crucial mitotic factors and events to mitochondrial dynamics and which could be implicated in human disease.

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“…33 CDKs are central regulators of the cell cycle including processes of DNA replication, DNA repair, chromosome segregation, and mitotic exit. 34,35 Cyclin B1/CDK1 regulates mitosis G2-M phase transition, during which CDK1 is controlled by checkpoint kinases to prevent aberrant DNA distributed to daughter cells. 34 MCM 2-7 proteins function as a helicase complex composing pre-replication complexes (pre-RCs), which license the initiation of DNA replication.…”

Section: Dovepressmentioning

confidence: 99%

“…34,35 Cyclin B1/CDK1 regulates mitosis G2-M phase transition, during which CDK1 is controlled by checkpoint kinases to prevent aberrant DNA distributed to daughter cells. 34 MCM 2-7 proteins function as a helicase complex composing pre-replication complexes (pre-RCs), which license the initiation of DNA replication. Phosphorylation of CDKs can activate pre-RCs at the onset of DNA replication and inhibit pre-RCs reassembling to block rereplication.…”

Section: Dovepressmentioning

confidence: 99%

ZWINT is a Promising Therapeutic Biomarker Associated with the Immune Microenvironment of Hepatocellular Carcinoma

Lin

Zhang

Lin

et al. 2021

IJGM

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“…Progress from G 0 to G 1 and through the G 1 phase of the mammalian cell cycle is mediated by the cyclin-dependent kinases 4 and 6 (CDK4, CDK6), which are activated through binding with their regulatory subunits D-type cyclins (D1, D2, and D3) (1)(2)(3)(4). It is widely accepted that CDK4 regulates critical aspects of the cell cycle via phosphorylation of the retinoblastoma (Rb) family of proteins (5,6).…”

Section: Introductionmentioning

confidence: 99%

CDK4 has the ability to regulate Aurora B and Cenpp expression in mouse keratinocytes

Lee

Rodriguez²,

Majumdar

et al. 2021

Oncol Lett

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Cyclin-dependent kinase 4 (CDK4) is a critical molecule that regulates key aspects of cell proliferation through phosphorylation of the retinoblastoma (Rb) family of proteins. In the last few years, it has been suggested that CDK4 plays alternative roles in cell proliferation and tumorigenesis. The main aim of the present study was to define a novel CDK4 function as a transcriptional regulator of genes involved in chromosome segregation, contributing to the G 2 /M phase transition. Herein, chromatin-immunoprecipitation reverse transcription-quantitative PCR assays were performed to demonstrate that CDK4 could occupy the promoter region of genes associated with chromosomal segregation, such as Aurora-B (Aurkb) and Centromere Protein P (CENP-P). Moreover, gain- and loss-of-function experiments showed that CDK4 participated in the transcriptional regulation of Aurkb and CENP-P. The finding that Aurkb may have a crucial role in chromosome bi-orientation and the spindle assembly checkpoint, and that CENP-P could be required for proper kinetochore function suggests that dysregulation of CDK4 expression induces chromosomal instability and, in some cases, cancer development.

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Cyclin-Dependent Kinases (CDK) and Their Role in Diseases Development–Review

Cited by 36 publications

References 333 publications

TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy

The Multifaceted Regulation of Mitochondrial Dynamics During Mitosis

ZWINT is a Promising Therapeutic Biomarker Associated with the Immune Microenvironment of Hepatocellular Carcinoma

CDK4 has the ability to regulate Aurora B and Cenpp expression in mouse keratinocytes

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