Identification of regulatory regions within the KAI1 promoter: a role for binding of AP1, AP2 and p53

Marreiros, Alexandra; Czolij, R.; Yardley, Gina; Crossley, Merlin; Jackson, Paul

doi:10.1016/s0378-1119(02)01101-0

Cited by 30 publications

(31 citation statements)

References 24 publications

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“…ATF3 can form a complex with various other members in the ATF family such as ATF2 and ATF4, as well as AP-1 proteins (27,28). Interestingly, we found that ATF3, in combination with the AP-1 family protein JunB, significantly enhanced KAI1 transcriptional activity compared with each alone (Fig.…”

Section: Ndrg1 Up-regulates Expression Of Kai1 Gene In Prostatementioning

confidence: 69%

“…Previously, we showed that p53 is able to bind to the KAI1 promoter and turn on its transcription (21,22). Other molecules involved in KAI1 transcriptional regulation include NFB, ␤-catenin/Reptin, Tip60/Fe65, N-CoR/TAB2/HDAC3 and AP-1 (23)(24)(25)(26)(27)(28). Interestingly, these transcription factors were frequently found to coordinately regulate the expression of KAI1 as either co-activator or co-repressor.…”

mentioning

confidence: 98%

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KAI1 Gene Is Engaged in NDRG1 Gene-mediated Metastasis Suppression through the ATF3-NFκB Complex in Human Prostate Cancer

Iiizumi‐Gairani

Okuda

et al. 2011

Journal of Biological Chemistry

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Section: Ndrg1 Up-regulates Expression Of Kai1 Gene In Prostatementioning

confidence: 69%

mentioning

confidence: 98%

KAI1 Gene Is Engaged in NDRG1 Gene-mediated Metastasis Suppression through the ATF3-NFκB Complex in Human Prostate Cancer

Iiizumi‐Gairani

Okuda

et al. 2011

Journal of Biological Chemistry

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“…AP-2-regulated genes include c-Kit, which regulates cellular proliferation and differentiation ; MUC18 (melanoma-associated glycoprotein), an adhesion molecule involved in angiogenesis ; MMP-2 (matrix metalloproteinase-2), which is involved in invasion (Bar-Eli, 2001); and KAI1 (prostate cancer antimetastasis gene 1), a prostate-specific metastasis suppressor (Marreiros et al, 2003). When AP-2 is lost, less c-Kit and KAI1, but more MUC18 and MMP2, are produced, resulting in a cell's increased potential to grow and divide uncontrollably Jean et al, 1998;Bar-Eli, 2001;Marreiros et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…When AP-2 is lost, less c-Kit and KAI1, but more MUC18 and MMP2, are produced, resulting in a cell's increased potential to grow and divide uncontrollably Jean et al, 1998;Bar-Eli, 2001;Marreiros et al, 2003). It has been reported that AP-2a overexpression can reduce thymidine incorporation and 5-bromo-2 0 -deoxyuridine incorporation, which are indicators of DNA synthesis (Wajapeyee and Somasundaram, 2003).…”

Section: Introductionmentioning

confidence: 99%

AP-2α and AP-2γ are transcriptional targets of p53 in human breast carcinoma cells

Watts

Oshiro

et al. 2006

Oncogene

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Activating enhancer-binding protein 2a (AP-2a) and activating enhancer-binding protein 2c (AP-2c) are transcription factors that bind GC-rich consensus sequences and regulate the expression of many downstream genes. AP-2a and AP-2c interact with p53 both physically and functionally. Expression microarray results in human breast carcinoma cells with forced p53 expression revealed AP-2c as a putative transcriptional target of p53. To confirm and extend these findings we measured the effects of forced p53 expression in human breast carcinoma cells by real-time reverse transcription-PCR, Western blotting, electrophoretic gel mobility shift assays, promoter reporter, chromatin immunoprecipitation and chromatin accessibility assays. Wild-type p53 expression rapidly induced not only AP-2c but also AP-2a mRNA. The subsequent increase in these proteins led to increased AP-2 DNAbinding and transactivating activity. Candidate p53-binding sites were identified in the AP-2a and AP-2c promoters. p53 binding to these cis-elements in vivo was also observed, together with a relaxation of chromatin structure in these regions. Finally, expression of either AP-2a or c inhibited growth of human breast carcinoma cells in vitro. Taken together, our findings indicate that these AP-2 genes are targets for transcriptional activation by p53 and suggest that AP-2 proteins may mediate some of the downstream effects of p53 expression such as inhibition of proliferation.

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“…Total RNA was isolated from the cells using TriReagent according to the manufacturer's instructions (Invitrogen Australia, Mulgrave, VIC, Australia): 5 mg were reverse-transcribed and subjected to hotstart PCR using previously published primers for OPG (548 bp amplicon), 14 AR 22 and the housekeeping gene, glyceraldehyde 3-phosphate dehydrogenase (GAPdH). 23 PCR analysis of PC-3 and LNCaP-FGC OPG mRNA was performed at 25 and 28 cycles, respectively, in the linear phase of amplification. Linear amplification of GAPdH used 21 cycles.…”

Section: Rt-pcrmentioning

confidence: 99%

Androgen decreases osteoprotegerin expression in prostate cancer cells

Vandyke

Jackson

Rowe

et al. 2006

Prostate Cancer Prostatic Dis

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Osteoprotegerin (OPG), a key regulator of bone resorption, is hypothesized to have a role in prostate cancer (CaP) bone metastasis. As advanced CaP is treated by androgen ablation, we examined if androgen modulates OPG expression by CaP cell lines in vitro. Basal levels of secreted OPG protein were significantly greater in androgen-independent PC-3 cells compared with androgen-responsive LNCaP-FGC cells (Po0.001); OPG was not detected in the androgenresponsive CaP cell lines LAPC-4 or DuCaP. Treatment with 5a-dihydrotestosterone (5a-DHT) significantly decreased OPG protein levels in both PC-3 and LNCaP-FGC, with maximal suppression using 10 À9 -10 À7 M 5a-DHT in PC-3 (Po0.01; day 3), and using 10 À10 -10 À9 M 5a-DHT in LNCaP-FGC cells (Po0.01; day 6). OPG messenger RNA levels were not significantly altered by this 5a-DHT treatment. Co-treatment with 10 À6 M flutamide blocked 5a-DHT inhibition of OPG protein expression in LNCaP-FGC cells. These data suggest that androgen may modulate OPG protein levels in CaP cells lines in vitro using a post-transcriptional mechanism.

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Identification of regulatory regions within the KAI1 promoter: a role for binding of AP1, AP2 and p53

Cited by 30 publications

References 24 publications

KAI1 Gene Is Engaged in NDRG1 Gene-mediated Metastasis Suppression through the ATF3-NFκB Complex in Human Prostate Cancer

KAI1 Gene Is Engaged in NDRG1 Gene-mediated Metastasis Suppression through the ATF3-NFκB Complex in Human Prostate Cancer

AP-2α and AP-2γ are transcriptional targets of p53 in human breast carcinoma cells

Androgen decreases osteoprotegerin expression in prostate cancer cells

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