ArticleTumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine2012
Analysis of human Ki-67 gene promoter and identification of the Sp1 binding sites for Ki-67 transcription.
Article in Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- The intrinsically disorderly story of Ki-67.Open biology · 2021Review
- Dysregulation of Ki-67 Expression in T Cells of Children with Autism Spectrum Disorder.Children (Basel, Switzerland) · 2021Article
- Reciprocal Role Of DNA Methylation And Sp1 Binding In Ki-67 Gene Transcription.Cancer management and research · 2019Article
- Ki67 targeted strategies for cancer therapy.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2018Review
- Potent anti-tumour activity of a novel conditionally replicating adenovirus for melanoma via inhibition of migration and invasion.British journal of cancer · 2014Article
- A dual-regulated oncolytic adenovirus expressing interleukin-24 sensitizes melanoma cells to temozolomide via the induction of apoptosis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2013Article
- IRF1 suppresses Ki-67 promoter activity through interfering with Sp1 activation.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ki-67 as a cell proliferation marker is tightly associated with maintenance and regulation of the cell division. To understand the mechanism of Ki-67 gene expression and regulation, we first cloned 5'-flanking region and identified the Ki-67 core promoter. The deletion analysis and the dual luciferase reporter assay were used to locate the Ki-67 core promoter from -223 to +12 nt relative to the transcriptional initiation site, which is the TATA less, GC rich region comprised of several putative Sp1 binding sites. Compared with the hTERT promoter and Survivin promoter, the Ki-67 core promoter possessed higher transcription activity and more desirable tumor selectivity. In order to further demonstrate the contribution of transcription factor Sp1 on regulating the Ki-67 gene transcription, we confirmed three Sp1 binding sites from -170 to -145 nt, from -63 to -38 nt, and from -14 to +12 nt existed in the Ki-67 core promoter by the supershift assay. The deletion mutagenesis, together with the dual luciferase reporter assay, indicated that these Sp1 binding sites, particularly the region from -170 to -145 nt, were involved in positive regulation of the Ki-67 gene expression. Collectively, it was demonstrated that the region from -223 to +12 nt could drive the transcription of the Ki-67 gene, and the Sp1 binding site is essential to transcriptional regulation of the Ki-67 gene.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.