We found that Steroid receptor coactivator 1 overexpression potentiates cell growth stimulated by E2 in accordance with enhancement of transcriptional activation of exogenous and endogenous E2-responsive genes
2002
Key concepts
- endogenous
- pancreatic ductal adenocarcinoma
- lipophilic
- proliferating cell nuclear antigen
- exogenous
- bisphenol A
- hepatocellular carcinoma
- estrogen receptor
- cell growth
- MCF-7
- vitamins
- Steroid receptor coactivator 1
- cleavage and polyadenylation specificity factor
- Chronic intestinal pseudo-obstruction
- messenger RNA
Scholarcy highlights
- Steroid hormones regulate cell growth and function through the transcriptional control of target genes by their cognate nuclear receptors
- We found that Steroid receptor coactivator 1 overexpression potentiates cell growth stimulated by E2 in accordance with enhancement of transcriptional activation of exogenous and endogenous E2-responsive genes
- These findings clearly indicate the importance of nuclear receptor coactivators for the activities of steroid/lipophilic vitamins in cell growth and gene expression
- We report that SRC-1 was overexpressed in 25 of 40 human hepatocellular carcinoma specimens
- The SRC-1/ER-α complex is supposed to potentiate E2-stimulated MCF-7 cell growth by enhancing the transcriptional activation of many exogenous and endogenous E2-responsive genes, including cyclin D1a and Mucin, which are both overexpressed in breast cancer and involved in the SRC-1/ER-α-related proliferation-enhancing pathways
- Stable expression of the exogenous Krüppel-like factor 6 was sufficient to abrogate the pro-survival effects of miR-342-3p in GEM-treated pancreatic ductal adenocarcinoma cells. These results suggest that leptin-elicited miR-342-3p upregulation mediates, at least partially, the GEM resistance through inhibition of KLF6 signaling in PDAC
- In contrast to other factors that regulate termination by binding to specific signals on nascent RNA, the RDC complex inhibits termination in a chromatin-dependent and sequence-independent manner
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