What is the role of cyclin D1 in cell‑cycle regulation?

Medical Advisory BoardAll articles are reviewed for accuracy by our Medical Advisory Board
Educational purpose only • Exercise caution as content is pending human review
Article Review Status
Submitted
Under Review
Approved

Last updated: February 20, 2026View editorial policy

Personalize

Help us tailor your experience

Which best describes you? Your choice helps us use language that's most understandable for you.

Cyclin D1: Role in Cell Cycle Regulation

Cyclin D1 functions as a critical regulator of the G1 to S phase transition in the cell cycle by forming complexes with cyclin-dependent kinases (CDK4/6) that phosphorylate retinoblastoma protein (Rb), thereby releasing E2F transcription factors to drive cell cycle progression. 1

Primary Cell Cycle Function

Mechanism of Action:

  • Cyclin D1 binds to CDK4 or CDK6 to form active holoenzyme complexes 2, 3
  • These CyclinD:Cdk4/6 complexes phosphorylate Rb and other pocket family proteins 1, 4
  • Phosphorylation of Rb releases E2F1-3/DP1-2 transcription factors from inhibitory complexes 1
  • Released E2F transcription factors activate transcription of dozens of genes required for S phase entry 1

Target Genes Activated:

  • Positive cell cycle regulators: CCND1 (cyclin D1 itself), CCND3, CCNE1, CCNE2, CDC25A, CDK2, MYC, MYCN, JUN, E2F1-3, NPAT, MYB, MYBL2, and TFDP1 1
  • Negative cell cycle regulators: CDKN1C, CDKN2C, CDKN2D, E2F4-8, RB1, RBL1, and TP53 1

Feedback Loop Regulation

Positive Feedback:

  • CyclinE:Cdk2 further phosphorylates pocket proteins, promoting transcription of more Cyclin D and E, creating an amplification loop that reinforces G1-S progression 1
  • This positive feedback initially drives the cell irreversibly toward S phase commitment 1

Negative Feedback Termination:

  • E2F6-8 transcription (downstream of E2F1-3) represses the same promoters previously activated by E2F1-3 1
  • CyclinE:Cdk2 phosphorylates E2F1-3, causing detachment from promoters 1
  • SKP2 protein (an E2F1-3 target) participates in ubiquitin-mediated degradation of E2F1-3 1

CDK-Independent Functions

Beyond Cell Cycle Control:

  • Cyclin D1 regulates transcription factors, coactivators, corepressors, histone acetylation, and chromatin remodeling proteins independent of CDK activity 3
  • Cell migration and invasion: Cyclin D1 interacts with filamin A (FLNa) and affects phosphorylation at Ser2152 and Ser1459, modulating breast cancer cell motility 2
  • DNA repair checkpoint: Down-regulation of cyclin D1 is necessary for PCNA relocation and repair DNA synthesis; overexpression prevents DNA repair and blocks S phase entry 5
  • Cellular metabolism and differentiation: Cyclin D1 governs fat cell differentiation and metabolic processes 3

Protein Degradation Pathway

Selective Autophagy:

  • Cyclin D1 is selectively recruited and degraded through autophagy mediated by SQSTM1 (p62) after ubiquitination 1
  • This degradation pathway is particularly relevant in hepatocellular carcinoma where cyclin D1 is overexpressed 1

Clinical Significance in Cancer

Oncogenic Role:

  • Cyclin D1 overexpression or CCND1 gene amplification occurs in multiple cancers including breast, colon, prostate, parathyroid adenoma, lymphoma, and melanoma 2, 3, 6
  • Overexpression drives uncontrolled cellular proliferation and is associated with tumor invasion and metastasis 6
  • Cytoplasmic membrane localization (not just nuclear) correlates with tumor invasion and metastasis 6
  • Therapeutic targeting: CDK4/6 inhibitors (palbociclib, abemaciclib) block cyclin D1-CDK4/6 activity, showing clinical efficacy in mantle cell lymphoma with 18% overall response rate 4

Critical Timing

The G0-G1 transition involving cyclin D1 activity occurs rapidly (30-60 minutes) and consists primarily of post-translational modifications like phosphorylation/dephosphorylation 1. The subsequent 4 hours of G1 phase involve transcription and translation of proteins required for S phase entry 1.

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

Have a follow-up question?

Our Medical A.I. is used by practicing medical doctors at top research institutions around the world. Ask any follow up question and get world-class guideline-backed answers instantly.