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Transgenic overexpression of SRC-3 in mice causes spontaneous lung tumor formation [74]. SRC-3 gene amplification and protein overproduction were shown in as high as 27 % of non-small cell lung cancers (NSCLCs) in one study [115]; overexpression correlates with poor disease free and overall survival. Interestingly, ERK3, a kinase that phosphorylates SRC-3 and confers SRC-3 pro-invasive activity in lung cancer cells, was shown to be highly upregulated in lung cancer [108]. Overexpression of SRC-3 protein in lung cancer also was reported in two other studies [139, 140].

Oncogene 20:3047–3054 23. Kraus WL, Manning ET, Kadonaga JT (1999) Biochemical analysis of distinct activation functions in p300 that enhance transcription initiation with chromatin templates. Mol Cell Biol 19:8123–8135 24. Demarest SJ, Martinez-Yamout M, Chung J, Chen H, Xu W, Dyson HJ, Evans RM, Wright PE (2002) Mutual synergistic folding in recruitment of CBP/p300 by p160 nuclear receptor coactivators. Nature 415:549–553 25. Koh SS, Chen D, Lee YH, Stallcup MR (2001) Synergistic enhancement of nuclear receptor function by p160 coactivators and two coactivators with protein methyltransferase activities.

G. E2/ERα) signaling and epidermal growth factor signaling pathways [81]. g. tamoxifen, an estradiol antagonist, and letrozole, an antiaromatase inhibitor) have been commonly used for treating ER/PR-positive breast cancers. However, antihormone resistance (either naïve or acquired resistance after therapy) and associated cancer recurrence have been major obstacles for curing breast cancer patients. The acquisition of resistance to antihormonal drugs is often associated with a transition of hormone signaling-dependent to growth factor signaling-dependent tumor growth [121, 122].

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