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Last update 08 May 2025

CDK3

Last update 08 May 2025

Basic Info

Synonyms

CDK3, CDKN3, Cell division protein kinase 3

+ [2]

Introduction

Serine/threonine-protein kinase that plays a critical role in the control of the eukaryotic cell cycle; involved in G0-G1 and G1-S cell cycle transitions. Interacts with CCNC/cyclin-C during interphase. Phosphorylates histone H1, ATF1, RB1 and CABLES1. ATF1 phosphorylation triggers ATF1 transactivation and transcriptional activities, and promotes cell proliferation and transformation. CDK3/cyclin-C mediated RB1 phosphorylation is required for G0-G1 transition. Promotes G1-S transition probably by contributing to the activation of E2F1, E2F2 and E2F3 in a RB1-independent manner.

Drugs associated with CDK3

CDK3 inhibitors(Senex)

Target

CDK3

Mechanism

CDK3 inhibitors

Active Org.

Senex Biotechnology, Inc.

Originator Org.

Senex Biotechnology, Inc.

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NVP-LCQ195

Target

CDK1 x CDK2 x CDK3 x CDK5 x CDK9

Mechanism

CDK1 inhibitors [+4]

Active Org.-

Originator Org.

Astex Therapeutics Ltd.

Active Indication-

Inactive Indication

Multiple Myeloma

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

NEOS-518

Target

CDK1 x CDK2 x CDK3 x CDK9

Mechanism

CDK1 inhibitors [+3]

Active Org.-

Originator Org.

Neosome Life Sciences LLC

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CDK3

100 Translational Medicine associated with CDK3

0 Patents (Medical) associated with CDK3

127

Literatures (Medical) associated with CDK3

01 Apr 2025·Molecular Diversity

Identification of the potential Pan-CDK antagonists: tracing the path of virtual screening and inhibitory activity on lung cancer cells

Article

Author: Zhou, Yong ; Guan, Cha-Xiang ; Zhang, Jun ; Tao, Jia-Hao ; Ruan, Ping-Lang

Cyclin-dependent kinases (CDKs) are overexpressed in tumor cells, and their aberrant activation can promote the progression of non-small-cell lung cancer (NSCLC). We utilized structure-based virtual screening and experimental validation to screen for potential CDKs antagonists among TargetMol natural products. Molecular docking and molecular dynamics simulation results indicate that Dolastatin 10 exhibits strong interactions with multiple subtypes of CDKs (CDK1, CDK2, CDK3, CDK4, and CDK6), forming stable CDKs-Dolastatin 10 complex compounds. Furthermore, in vitro experiments demonstrate that Dolastatin 10 significantly inhibits the viability, migration, and invasion of H1299 cells in a concentration-dependent manner, arresting the cell cycle at the G2/M phase by inducing cell senescence. These findings suggest that Dolastatin 10 may serve as a potential CDKs antagonist deserving further investigation.

27 Mar 2025·Journal of Applied Biomedicine

Chemical composition and anticancer activity of Psychotria montana on MCF7 breast cancer cells: insights from in vitro (2D & 3D) studies and in silico analysis

Article

Author: Van Hung, Hoang ; Nguyen, Phu Hung ; Hoang, Viet ; Le, Thi Thanh Huong ; Kieu Oanh Nguyen, Thi

AIMThis study aimed to investigate the phytochemical composition of Psychotria montana extract (PME) and evaluate its inhibitory effects on MCF7 breast cancer cells.METHODSThe chemical composition of PME was analyzed using UPLC-QToF-MS. The effects of PME on cell proliferation were evaluated using the MTT assay. Flow cytometry was used for cell cycle and apoptosis analysis. The effects of PME on the transcription of cell cycle control genes were assessed using real-time PCR.RESULTSUPLC-QToF-MS analysis revealed major compounds of PME, including terpenoids and flavonoids, with the potential to inhibit proliferation, migration, and induce apoptosis in MCF7 cancer cells. PME effectively suppressed MCF7 cell proliferation under 2D culture, with a low IC50 value of 34.7 µg/ml. PME also hindered cell migration (p < 0.01) and reduced spheroid number (p < 0.001) and size (p < 0.001) in serum-free 3D culture. Apoptosis analysis via nuclear staining with DAPI and flow cytometry revealed an increase in the number of apoptotic cells after PME treatment (p < 0.001). Additionally, the PME induced cell cycle arrest at the G0/G1 phase (p < 0.05). PME altered the expression of cell cycle control genes (cyclins and CDKs) as well as cancer suppressor genes including p16, p27, and p53 at the transcriptional level (mRNA). The results of molecular docking suggest that the compounds present in PME exhibit a high binding affinity for CDK3, CDK4, CDK6, and CDK8 proteins, which are essential regulators of the cell cycle.CONCLUSIONPsychotria montana has the potential to inhibit cancer cells by inducing apoptosis and halting the cell cycle of MCF7 breast cancer cells.

01 Mar 2025·Translational Cancer Research

Scoparone suppresses proliferation and cell cycle of hepatocellular carcinoma cells via inhibiting AKT/GSK-3β/cyclin D1 signaling pathway

Article

Author: Yu, Song ; Wang, Gang ; Hong, Mei ; Liu, Weikang ; Zhu, Hao ; Zhang, Pengyu ; Shen, Genhai ; Gao, Quangen ; Li, Bin

BackgroundHepatocellular carcinoma (HCC) ranks as the sixth most prevalent cancer and the fourth leading cause of cancer-related mortality globally. Scoparone, a natural coumarin derivative primarily derived from Artemisia Capillaris Thunb, has demonstrated antitumor properties across various cancer types. However, its functions in HCC have not been clearly elucidated. This study aimed to investigate the antitumor effects of scoparone on the MHCC-97L and HCCC-9810 HCC cell lines.MethodsCell proliferation was assessed through viability and colony formation assays. Migration and invasion capabilities of the cells were evaluated by wound healing assays and Transwell assays. Additionally, transcriptome sequencing and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were conducted to uncover pathways linked to gene enrichment in the artemisinin treatment group. Western blotting and flow cytometry were utilized to analyze the expression of mechanistic proteins associated with artemisinin treatment in HCC.ResultsOur findings revealed that scoparone effectively inhibited the proliferation, migration, and invasion of HCC cells. The genes affected by scoparone treatment were predominantly enriched in pathways related to the cell cycle. Specifically, scoparone reduced the expression of genes such as CDK2, CDK3, CDK4, CDC25A, CCND1, and CCNE1, while it increased the expression of CDKN1A (p21). Furthermore, scoparone suppressed the levels of cell cycle-related proteins CDK2, CDK4, and cyclin D1, along with the signaling pathways involving p-AKT and p-GSK-3β. Notably, the inhibitory effects of scoparone on HCC cell proliferation were partially reversed by the AKT activator, SC79.ConclusionsScoparone inhibited HCC cell viability by targeting the AKT/GSK-3β/cyclin D1 pathway.

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