Different cyclins exhibit distinct expression and degradation patterns which contribute to the temporal coordination of each mitotic event.

This cyclin forms a complex with and functions as a regulatory subunit of CDK4 or CDK6, whose activity is required for cell cycle G1/S transition.

Mutations, amplification and overexpression of this gene, which alters cell cycle progression, are observed frequently in a variety of tumors and may contribute to tumorigenesis.

[18] Cyclin D1-CDK4 inhibits pRb through phosphorylation, allowing E2F transcription factors to transcribe genes required for entry into the S phase.

Increasing cyclin D1 levels during the G1 phase is induced by mitogenic growth factors [27] primarily through Ras-mediated pathways,[28][29][30] and hormones.

[32] Cyclin D1 overexpression has been shown to correlate with early cancer onset and tumor progression [19] and it can lead to oncogenesis by increasing anchorage-independent growth and angiogenesis via VEGF production.

[33] Cyclin D1 overexpression can also down-regulate Fas expression, leading to increased chemotherapeutic resistance and protection from apoptosis.