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Cyclin D1 overexpression has been shown to correlate with early cancer onset and tumor progression  and it can lead to oncogenesis by increasing anchorage-independent growth and angiogenesis via VEGF production.  Cyclin D1 overexpression can also down-regulate Fas expression, leading to increased chemotherapeutic resistance and protection from apoptosis.
Takano Y, Takenaka H, Kato Y, Masuda M, Mikami T, Saegusa M, Okayasu I. Cyclin D1 overexpression in invasive breast cancers: correlation with cyclin-dependent kinase 4 and oestrogen receptor overexpression, and lack of correlation with mitotic activity. J Cancer Res Clin Oncol. 1999;125:505–512. doi: 10. 1007/s004320050309.
Overexpression of cyclin D1 has also been linked to the development of endocrine resistance in breast cancer cells [20–22]. Cyclin D1 overexpression is a common event in cancer but does not occur solely as a consequence of gene amplification. Rather, increased levels of cyclin D1 frequently result from its defective regulation at the post-translational level [23, 24]. A number of therapeutic agents have been observed to induce cyclin D1 degradation in vitro [25–30].
Data from cancer studies have already identified that cyclin E1 and E2 are frequently not co-expressed in tumours, and may have distinct associations with recurrent disease. A likely explanation for the discordant expression of cyclin E1 and E2 in cancer is their regulation by distinct subsets of transcription factors and miRNAs. The expression of cyclin E2, independently of cyclin E1, can be induced via cyclin D1, Chd8 and CDP/Cux, all of which are upregulated in cancers [47, 123], and cyclin E2 is also independently suppressed by the tumour suppressor p53 . The co-regulation of cyclin E1 and cyclin E2 with distinct gene sets could explain the different relationship of each gene to disease. For example, cyclin E2, which is a target of cyclin D1 and Chd8 in estrogen-responsive cells , has been associated with poor outcome only in ER-positive breast cancers , which resembles the association of cyclin D1 overexpression.