BACKGROUND: In breast cancer, estrogen receptors have been demonstrated to interact with transcription factors to regulate target gene expression. However, high-throughput identification of the transcription regulation relationship between transcription factors and their target genes in response to estradiol is still in its infancy. PURPOSE: Thus, the objective of our study was to interpret the transcription regulation network of MCF7 breast cancer cells exposed to estradiol. METHODS: In this work, GSE11352 microarray data were used to identify differentially expressed genes (DEGs). RESULTS: Our results showed that the MYB (v-myb myeloblastosis viral oncogene homolog [avian]), PGR (progesterone receptor), and MYC (v-myc myelocytomatosis viral oncogene homolog [avian]) were hub nodes in our transcriptome network, which may interact with ER and, in turn, regulate target gene expression. MYB can up-regulate MCM3 (minichromosome maintenance 3) and MCM7 expression; PGR can suppress BCL2 (B-cell lymphoma 2) expression; MYC can inhibit TGFB2 (transforming growth factor, beta 2) expression. These genes are associated with breast cancer progression via cell cycling and the TGFβ signaling pathway. CONCLUSION: Analysis of transcriptional regulation may provide a better understanding of molecular mechanisms and clues to potential therapeutic targets in the treatment of breast cancer.
BACKGROUND: In breast cancer, estrogen receptors have been demonstrated to interact with transcription factors to regulate target gene expression. However, high-throughput identification of the transcription regulation relationship between transcription factors and their target genes in response to estradiol is still in its infancy. PURPOSE: Thus, the objective of our study was to interpret the transcription regulation network of MCF7 breast cancer cells exposed to estradiol. METHODS: In this work, GSE11352 microarray data were used to identify differentially expressed genes (DEGs). RESULTS: Our results showed that the MYB (v-mybmyeloblastosis viral oncogene homolog [avian]), PGR (progesterone receptor), and MYC (v-mycmyelocytomatosis viral oncogene homolog [avian]) were hub nodes in our transcriptome network, which may interact with ER and, in turn, regulate target gene expression. MYB can up-regulate MCM3 (minichromosome maintenance 3) and MCM7 expression; PGR can suppress BCL2 (B-cell lymphoma 2) expression; MYC can inhibit TGFB2 (transforming growth factor, beta 2) expression. These genes are associated with breast cancer progression via cell cycling and the TGFβ signaling pathway. CONCLUSION: Analysis of transcriptional regulation may provide a better understanding of molecular mechanisms and clues to potential therapeutic targets in the treatment of breast cancer.
Authors: Sanne Løkkegaard; Daniel Elias; Carla L Alves; Martin V Bennetzen; Anne-Vibeke Lænkholm; Martin Bak; Morten F Gjerstorff; Lene E Johansen; Henriette Vever; Christina Bjerre; Tove Kirkegaard; Bo Nordenskjöld; Tommy Fornander; Olle Stål; Linda S Lindström; Laura J Esserman; Anne E Lykkesfeldt; Jens S Andersen; Rikke Leth-Larsen; Henrik J Ditzel Journal: NPJ Breast Cancer Date: 2021-01-04