The T47D cell line is an ideal experimental model to elucidate the progesterone-specific effects of a luminal A subtype of breast cancer.
Cell lines are often used as in vitro tools to mimic certain types of in vivo system; several cell lines, including MCF-7 and T47D, have been widely used in breast cancer studies without investigating the cell lines' characteristics. In this study, we compared the genome-wide binding profiles of ERα, PR, and P300, and the gene expression changes between MCF-7 and T47D cell lines that represent the luminal A subtype of breast cancer. Surprisingly, several thousand genes were differentially expressed under estrogenic condition. In addition, ERα, PR, and P300 binding to regulatory elements showed distinct genomic landscapes between MCF-7 and T47D cell lines in the same hormonal states. In particular, the T47D cell line was markedly susceptible to progesterone, whereas the MCF-7 cell line did not respond to progesterone in the presence of estrogen. Consistently, changes in the expression level of the PR-target gene, STAT5A, were only observed in the T47D cell line, not the MCF-7 cell line, when treated with progesterone. Overall, the results highlight the importance of selecting appropriate cell lines for breast cancer studies and suggest that T47D cell lines can be an ideal experimental model to elucidate the progesterone-specific effects of a luminal A subtype of breast cancer.
Department of Clinical Laboratory Science, Semyung University, Jecheon 27136, Republic of Korea.
Sungryul
S
Yu
Department of Microbiology, College of Natural Sciences, Dankook University, Cheonan 31116, Republic of Korea.
Taemook
T
Kim
Department of Biological Sciences, Sookmyung Women's University, Seoul, 04310, Republic of Korea.
Kyung Hyun
KH
Yoo
Department of Microbiology, College of Natural Sciences, Dankook University, Cheonan 31116, Republic of Korea. Electronic address: kangk1204@dankook.ac.kr.
Keunsoo
K
Kang
D001665:Binding Sites; D001943:Breast Neoplasms / Q000235:genetics / Q000378:metabolism / Q000473:pathology; D045744:Cell Line, Tumor; D047628:Estrogen Receptor alpha / Q000235:genetics / Q000378:metabolism; D004967:Estrogens / Q000494:pharmacology*; D005260:Female; D020869:Gene Expression Profiling; D015972:Gene Expression Regulation, Neoplastic / Q000187:drug effects*; D055106:Genome-Wide Association Study; D006801:Humans; D061986:MCF-7 Cells; D008954:Models, Biological; D009928:Organ Specificity; D011374:Progesterone / Q000494:pharmacology*; D011485:Protein Binding; D011980:Receptors, Progesterone / Q000235:genetics / Q000378:metabolism; D050799:STAT5 Transcription Factor / Q000235:genetics / Q000378:metabolism; D059467:Transcriptome; D025521:Tumor Suppressor Proteins / Q000235:genetics / Q000378:metabolism; D050880:p300-CBP Transcription Factors / Q000235:genetics / Q000378:metabolism
C506487:ESR1 protein, human; D047628:Estrogen Receptor alpha; D004967:Estrogens; D011980:Receptors, Progesterone; D050799:STAT5 Transcription Factor; C494092:STAT5A protein, human; D025521:Tumor Suppressor Proteins; D011374:Progesterone; D050880:p300-CBP Transcription Factors
ERα; Estrogen receptor; MCF-7; PR; Progesterone receptor; T47D