Semistrong evidences
BCL2 expression has long been considered a good prognostic marker in breast cancer . DPN increased BCL2 mRNA and protein expression; likely by ERalpha activation because E2 regulates BCL2 transcription in MCF-7 cells via ERalpha- Sp1 and AP1 interactions , we can not conclude that the increase in BCL2 mRNA is due solely to E2-mediated decreased miR-21. View article
A highly GC-rich 39-bp region located 5819 bp upstream of the P1 promoter has been implicated in playing a major role in the regulation of BCL2 transcription . Multiple transcription factors have been reported to bind to or regulate BCL2 gene expression through this region, including CREB , WT1 , Sp1 , E2F , NF-kappaB , and NGF . For example, CREB functions to activate BCL2 expression , while WT1 functions to repress BCL2 expression . View article
Additionally, SP1 sites and a cAMP response element are necessary for estradiol-induced bcl-2 gene expression in MCF7 and T47D cells . View article
Because both ER-alpha and Sp1 DNA-binding and transactivating functions are needed for optimal estrogenic stimulation of genes such as PR and Bcl2, ER-positive breast cancers subjected to sufficient oxidative stress would be expected to exhibit suppressed expression of these estrogen-inducible genes. View article
Chromatin immunoprecipitation assays with antibodies specific for the NF-kappaB and CREB/ATF family members, as well as Sp1, resulted in the isolation of this IkappaBalpha-super-repressor responsive region of the bcl-2 promoter. View article
Further analysis demonstrated that the upstream region (-1603 to -1579) of the bcl-2 gene promoter contained two GC/GA-rich sites at -1601 (5 -GGGCTGG-3 ) and -1588 (3 -GGAGGG-5 ) that bound Sp1 protein. View article
In addition, two Sp1 binding sites in HS4 were also found to positively influence bcl-2 activity, and Sp1 was observed to interact with the human HS4 enhancer in vivo. View article
In conclusion, our results strongly indicate that up-regulation of uPAR expression by Bcl-2 in hypoxia is modulated by Sp1 DNA binding activity through the ERK signaling pathway. View article
In mechanism (ii) ER does not bind DNA. Examples of the tethering mechanism of ER transactivation include ERalpha interaction with Sp1 in conferring estrogen responsiveness on uteroglobin , RARalpha , insulin-like growth factor-binding protein-4 , transforming growth factor alpha , bcl-2 and the LDL receptor genes; ERalpha interaction with USF-1 and USF-2 in the cathepsin D promoter ; and ERalpha and ERbeta interaction with AP-1 . View article
In this work we demonstrated, for the first time, that Bcl-2 overexpression in cancer cells exposed to hypoxia modulates urokinase plasminogen activator receptor (uPAR) expression through Sp1 transcription factor and that the extracellular signal-regulated kinase (ERK) pathway plays a role in Sp1 transcriptional activity. View article
Mutation of Sp1 and C/EBPalpha binding sites reduced the TSA-induced repression of bcl-2 promoter activity. View article
Mutation of the CRE and the two Sp1 sites in different combinations in bcl-2 reporter constructs resulted in the loss of bcl-2 promoter repression by the IkappaBalpha-super-repressor. View article
P1 is known as the promoter having a predominant role in B cells and many transcription factors, such as cAMP response element-binding protein (CREB), Sp1, and NFkappaB, have been known to regulate transcription of Bcl-2 via the P1 promoter. View article
TSA treatment increased the acetylation of the transcription factors Sp1 and C/EBPalpha and decreased their binding as well as the binding of CBP and HDAC2 to the bcl-2 promoters. View article
The BCL-2 promoter can be regulated by several transcription factors that can functionally interact with ETS factors, including members of the CREB/ATF family, Sp1 and p53 . BCL-2 transcription in F-MuLV-induced erythroleukemia is therefore likely to depend upon the interaction between overexpressed FLI-1 and cofactors, the expression or activity of which may vary during disease progression. View article
The bcl-2 gene promoter comprises P1 and P2 regions and has characterized cis-elements viz., one CRE and two SP1 sites located upstream of the P1 promoter that determine the basal and inducible expression . View article
The plasmid LB170, used in our studies of the bcl-2 promoter, contains several binding sites for known transcriptional regulators of bcl-2, including Wilms Tumor 1, SP1, and cAMP response element binding proteins. View article
These results suggest that the interactions of the nuclear factor kappaB and Sp1 transcription factors with the immunoglobulin heavy chain enhancer region are important for bcl-2 deregulation in t(14;18) cells. View article
Transcription factors such as c-myc, Sp1, nuclear factor-kappaB (NF-kappaB) and upstream stimulatory factors (USF) have been shown to upregulate hTERT transcription whereas transcription factors like Mad1, Wilms tumor 1 (WT1) tumor suppressor protein, E2F, p53 and myeloid cell-specific zinc finger protein-2 (MZF-2) have been found to down-regulate hTERT transcription . Bcl-2, the oncoprotein involved in the inhibition of cellular apoptosis has also been reported to modulate telomerase activity . Several studies have implicated sex steroid hormones (estrogen, progesterone and androgens) in the regulation of hTERT transcription . View article
Treatment of cells with mitramycin A, an inhibitor of Sp1 activity, confirmed the role of Sp1 transcriptional activity in uPAR induction by Bcl-2. View article
We therefore conclude that the activation of bcl-2 by NF-kappaB in t(14;18) lymphoma cells is mediated through the CRE and Sp1 binding sites. View article
Weak evidences
For the three genes assessed (FOS, BCL2, and PGR), we found that E2 treatment increased their gene expression (mRNA level) and that Sp1 knock-down also reduced their gene expression after E2. View article
Moreover, using RNA interference with small inhibitory RNAs for Sp1, Sp3, and Sp4, we observed that curcumin-dependent inhibition of nuclear factor kappaB (NF-kappaB)-dependent genes, such as bcl-2, survivin, and cyclin D1, was also due, in part, to loss of Sp proteins. View article
Multiple initiation sites were also found in a GC-rich region with Sp1 binding motifs in exon I. Most t(14;18) breakpoints cluster within the 3 UT of Bcl-2 implicating that event in gene deregulation. View article
Similarly, miR-18b also has the potential to regulate multiple antiapoptotic genes, including Akt, Sp1, Bcl-2, E2F, and IGF1. View article
Treatment of 2F7 cells with Rituximab or the p38 inhibitor SB203580 inhibited the constitutive p38 MAPK activity and resulted in the inhibition of Sp1, IL-10, STAT3, and Bcl-2. View article