ArticleExperimental and therapeutic medicine2020
Suppression of α-methylacyl-coenzyme A racemase by miR200c inhibits prostate adenocarcinoma cell proliferation and migration.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Review
- The role of miR-200 family in the regulation of hallmarks of cancer.Frontiers in oncology · 2022Review
- Racemases and epimerases operating through a 1,1-proton transfer mechanism: reactivity, mechanism and inhibition.Chemical Society reviews · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Overexpression of α-methylacyl-coenzyme A racemase (AMACR/P504S) is a major abnormality that has been observed in prostate cancer, whereas microRNA (miRNA/miR) 200c, is downregulated. The aim of the present study was to explore whether miR200c was able to exert any regulatory effects on AMACR. To meet this aim, bioinformatics analysis was performed to identify potential binding sites for miR200c in the 3'-untranslated region (3'-UTR) of AMACR. Recombinant adenoviral and dual reporter gene assays were designed to examine the binding of miR200c to the potential seed sequences in the AMACR 3'-UTR. Conventional reverse transcription (RT)-PCR, RT-quantitative (q)PCR and western blotting were also used to examine the regulatory effects of miR200c on AMACR at the mRNA and protein levels. Furthermore, Cell Counting Kit-8, wound healing and Transwell assays were performed to investigate the biological effects of miR200c-AMACR deregulation on prostate cancer cell proliferation, migration and invasion. It was revealed that miR200c post-transcriptionally suppressed AMACR expression by interacting with the 90-97 nucleotide sequence of the AMACR mRNA 3'-UTR. Artificial overexpression of miR200c significantly downregulated the mRNA and protein levels of AMACR in DU145 and PC-3 prostate cancer cells. Knockdown of AMACR by RNA interference, or overexpression of miR200c by recombinant adenoviral Ad-miR200c, inhibited prostate cancer cell proliferation, migration and invasiveness. Taken together, the results of the present study revealed that miR200c may suppress the AMACR expression level post-transcriptionally. The results also indicate that perturbation of the miR200c-AMACR regulatory mechanism may be involved in prostate carcinogenesis and that this may be exploited in future therapeutic approaches to prostate cancer.
Indexed as
Identifiers
What OpenQuestion holds
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.