The Adipose Promoter 1.4 Responsible For Driving The...

The adipose promoter 1.4 is responsible for driving the transcription process at low levels in the adipose cells. Cytokines class 1 and TNFÃŽ ± are produced locally within the cells allows the regulation of the promoter, promoter II on the other hand is regulated by cAMP and gonadotropins (Goss, 2004). The adipose cells tend to utilize all the promoters (II, 1.3 and 1.7) in instances where breast cancer is involved owing to the cancerous cells. Switch of the promoters depending with the kind of environment leads to enhanced gene transcription of aromatase, the expression of the proteins and the enzymatic activity. Thus, explaining why there is a high presence of oestrogen surrounding breast cancer cells. Breast cancer cells tend to†¦show more content†¦The human aromatase gene is present in the haploid genome. Thus, the unique sequence can be denoted as shown in the figure below. Figure 2: Gene Structure (source: Esin, Yuce, Kilickap, and Erman (2013)) Post-transcriptional Regulation miRNA is involved in the translational regulation of a wide range of genes through the control of the translational rate of the transcript stability. Estrogen in the ovary has been shown to be regulated by miR-378, a miRNA that targets aromatase. Further the activity of aromatase is also controlled by post translational modifications that include glycosylation and phosphorylation. Post translational glycosylation occurs in the placental aromatase and causes an increase of about 35-40% in the activities of the enzyme. Further, the activities of aromatase can also be reduced and restored by phosphorylation and dephosphorylation respectively in cells. Similarly, the insulin related activities also enhance the processes of aromatase especially in breast cancer malignant and they are mediated by MARK and P13K/Akt providing the pathway of signal channels (Berstein, Santen, 2008). Breast Cancer Stroma It is crucial to illustrate that healthy cells in breast tissues tend to express low levels of aromatase transcriptions from exon 1.4. Once the cells in the breast turn to become carcinogenesis, the use of exon 1.4 is halted while exon 1.2 is used in the aromatase and