Estrogen-induced post-transcriptional modulation of c-myc proto-oncogene expression in human breast cancer cells.

Santos, George F.; Scott, Gary K.; Lee, W M; Liu, E; Benz, Christopher C.

doi:10.1016/s0021-9258(19)81551-x

Cited by 68 publications

(3 citation statements)

References 25 publications

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“…For miR‐17~92, various research groups have found that these miRNAs are regulated by oestrogen stimuli in vivo and in vitro . The molecule basis of the phenomenon has been described above for the co‐regulation effects of activated ESα (oestrogen‐binding ESα) and transcription factor c‐myc . Based on our results, we added new evidence that the expression of miR‐17~92 was modulated by oestrogen and then showed sex disparity in the liver.…”

Section: Discussionsupporting

confidence: 68%

MiR‐17~92 ablation impairs liver regeneration in an estrogen‐dependent manner

Zhou

Zhang

et al. 2016

J Cellular Molecular Medi

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As one of the most important post‐transcriptional regulators, microRNAs (miRNAs) participate in diverse biological processes, including the regulation of cell proliferation. MiR‐17~92 has been found to act as an oncogene, and it is closely associated with cell proliferation. However, its role in liver regeneration is still unclear. We generated a hepatocyte‐specific miR‐17~92‐deficient mouse and used a mouse model with 70% partial hepatectomy (PH) or intraperitoneal injection of carbon tetrachloride to demonstrate the role of MiR‐17~92 in liver regeneration. In quiescent livers, the expression of the miR‐17~92 cluster showed a gender disparity, with much higher expression in female mice. The expression of four members of this cluster was found to be markedly reduced after 70% PH. The ablation of miR‐17~92 led to obvious regeneration impairment during the early‐stage regeneration in the female mice. Ovariectomy greatly reduced miR‐17~92 expression but significantly promoted liver regeneration in wild‐type mice. In addition, early regeneration impairment in miR‐17~92‐deficient livers could be largely restored following ovariectomy. The proliferation suppressors p21 and Pten were found to be the target effectors of miR‐17~92. MiR‐17~92 disruption resulted in elevated protein levels of p21 and Pten in regenerating livers. MiR‐17~92 functions as a proliferation stimulator and acts in an oestrogen‐dependent manner. The loss of this miRNA results in increases in p21 and Pten expression and therefore impairs liver regeneration in female mice.

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Section: Discussionsupporting

confidence: 68%

MiR‐17~92 ablation impairs liver regeneration in an estrogen‐dependent manner

Zhou

Zhang

et al. 2016

J Cellular Molecular Medi

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“…In other experiments, small decreases in c-myc mRNA were consistently observed within 30 min of treatment (data not shown). These data are in accord with data obtained using other, structurally distinct antiestrogens (54,70). The changes in gene expression associated with growth arrest after antiestrogen treatment were thus compatible with a role for c-myc and cyclin Dl, and, to a lesser extent, cyclin E, in the control of breast cancer cell cycle progression by antiestrogens.…”

Section: Resultssupporting

confidence: 86%

Growth Factor, Steroid, and Steroid Antagonist Regulation of Cyclin Gene Expression Associated With Changes in T-47D Human Breast Cancer Cell Cycle Progression

Musgrove

Lee

et al. 1993

Molecular and Cellular Biology

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Cyclins and proto-oncogenes including c-myc have been implicated in eukaryotic cell cycle control. The role of cyclins in steroidal regulation of cell proliferation is unknown, but a role for c-myc has been suggested. This study investigated the relationship between regulation of T-47D breast cancer cell cycle progression, particularly by steroids and their antagonists, and changes in the levels of expression of these genes. Sequential induction of cyclins D1 (early G1 phase), D3, E, A (late G1-early S phase), and B1 (G2 phase) was observed following insulin stimulation of cell cycle progression in serum-free medium. Transient acceleration of G1-phase cells by progestin was also accompanied by rapid induction of cyclin D1, apparent within 2 h. This early induction of cyclin D1 and the ability of delayed administration of antiprogestin to antagonize progestin-induced increases in both cyclin D1 mRNA and the proportion of cells in S phase support a central role for cyclin D1 in mediating the mitogenic response in T-47D cells. Compatible with this hypothesis, antiestrogen treatment reduced the expression of cyclin D1 approximately 8 h before changes in cell cycle phase distribution accompanying growth inhibition. In the absence of progestin, antiprogestin treatment inhibited T-47D cell cycle progression but in contrast did not decrease cyclin D1 expression. Thus, changes in cyclin D1 gene expression are often, but not invariably, associated with changes in the rate of T-47D breast cancer cell cycle progression. However, both antiestrogen and antiprogestin depleted c-myc mRNA by > 80% within 2 h. These data suggest the involvement of both cyclin D1 and c-myc in the steroidal control of breast cancer cell cycle progression.

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“…The processing and polyadenylation signals from the vitellogenin B1 gene are positioned at the 3' end so that these transcripts will be properly polyadenylated in Xenopus cells. region in the estrogen regulation of c-myc mRNA (34). However, most studies have identified stem and loop structures (23,26,32), A+U-rich sequences (4,38), and other elements in the 3' untranslated region, as well as the length of the poly(A) tract available for interaction with the poly(A)-binding protein (8,24,25,37), as being major determinants of mRNA stability.…”

mentioning

confidence: 99%

Estradiol and Estrogen Receptor-Dependent Stabilization of a Mini-vitellogenin mRNA Lacking 5,100 Nucleotides of Coding Sequence

Nielsen

Shapiro

1990

Molecular and Cellular Biology

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We have developed a transfection assay to investigate the estrogen-mediated stabilization of cytoplasmic vitellogenin mRNA. A minivitellogenin (MV5) gene containing the 5' and 3' untranslated and coding regions but lacking 5,075 nucleotides of internal coding sequence was constructed. Cotransfection of the MV5 plasmid and a Xenopus estrogen receptor expression plasmid into Xenopus liver tissue culture cells yielded a 529-nucleotide MV5 mRNA, which was specifically stabilized by estrogen. MV5 mRNA exhibited the increased stability indicative of positive regulation when the estradiol-estrogen receptor complex was present and was not destabilized by unliganded estrogen receptor. Transfected estrogen receptor, estradiol, and 529 nucleotides of the 5,604-nucleotide vitellogenin B1 mRNA were sufficient for stabilization.

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Estrogen-induced post-transcriptional modulation of c-myc proto-oncogene expression in human breast cancer cells.

Cited by 68 publications

References 25 publications

MiR‐17~92 ablation impairs liver regeneration in an estrogen‐dependent manner

MiR‐17~92 ablation impairs liver regeneration in an estrogen‐dependent manner

Growth Factor, Steroid, and Steroid Antagonist Regulation of Cyclin Gene Expression Associated With Changes in T-47D Human Breast Cancer Cell Cycle Progression

Estradiol and Estrogen Receptor-Dependent Stabilization of a Mini-vitellogenin mRNA Lacking 5,100 Nucleotides of Coding Sequence

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