ArticleMolecular biology reports2009
Molecular cloning and preliminary analysis of the human alpha-methylacyl-CoA racemase promoter.
Article in Molecular biology reports, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Suppression of α-methylacyl-coenzyme A racemase by miR200c inhibits prostate adenocarcinoma cell proliferation and migration.Experimental and therapeutic medicine · 2020Article
- Article
- Induction of alpha-methylacyl-CoA racemase by miR-138 via up-regulation of β-catenin in prostate cancer cells.Journal of cancer research and clinical oncology · 2017Article
- High alpha-methylacyl-CoA racemase (AMACR) is associated with ERG expression and with adverse clinical outcome in patients with localized prostate cancer.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
- AMACR overexpression as a poor prognostic factor in patients with nasopharyngeal carcinoma.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2014Article
- Functional analysis of pig myostatin gene promoter with some adipogenesis- and myogenesis-related factors.Molecular and cellular biochemistry · 2012Article
- Cancer biomarker discovery: the entropic hallmark.PloS one · 2010Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alpha-methylacyl-CoA racemase (AMACR) is an enzyme involved in beta-oxidation of branched-chain fatty acids and bile acid intermediates. Recent works have revealed that AMACR is overexpressed in prostate cancer and functionally important for the growth of prostate cancer cells. Despite the recent interest in AMACR as a diagnostic marker for prostate cancer, little is known about the transcriptional regulation of AMACR in prostate cancer. To elucidate the regulation of the AMACR gene, a 2.3-kb fragment of its 5' flanking region was cloned into pGL3-Basic, then using tansfection and Dual-luciferase reporter assay, a preliminary analysis on promoter activity and function of this 2.3-kb sequence was carried out. This 2.3-kb fragment represented promoter activity that consistent with the expression level in LNCaP and PC-3 cells respectively. Transfection experiments of 5'-deletion mutants into LNCaP cells revealed a positive-regulatory region located between nucleotides -423 and -93 that may be responsible for AMACR transactivation in LNCaP cells. Cotransfection experiments revealed that promoter activity of this 2.3-kb sequence was down-regulated by C/EBPalpha, p53, NF-kappaB p50. And data from luciferase-based reporter assays suggest that the promoter function of AMACR is independent of androgen receptor-mediated signaling.
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Registered trials
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.