ArticleOncoTargets and therapy2017
Exploration of the molecular mechanism of prostate cancer based on mRNA and miRNA expression profiles.
Article in OncoTargets and therapy, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 15 citations in OpenAlex.
- The L-type calcium channel CaV1.3: A potential target for cancer therapy.Journal of cellular and molecular medicine · 2024Review
- Deregulated microRNAs Involved in Prostate Cancer Aggressiveness and Treatment Resistance Mechanisms.Cancers · 2023Review
- CACNA1D overexpression and voltage-gated calcium channels in prostate cancer during androgen deprivation.Scientific reports · 2023Article
- AZU1 (HBP/CAP37) and PRKCG (PKC-gamma) may be candidate genes affecting the severity of acute mountain sickness.BMC medical genomics · 2023Article
- Analysis of aberrant miRNA-mRNA interaction networks in prostate cancer to conjecture its molecular mechanisms.Cancer biomarkers : section A of Disease markers · 2022Article
- miR-593-3p Promotes Proliferation and Invasion in Prostate Cancer Cells by Targeting ADIPOR1.OncoTargets and therapy · 2021Article
- Cerina: systematic circRNA functional annotation based on integrative analysis of ceRNA interactions.Scientific reports · 2020Article
- Bioinformatics analysis of potential core genes for glioblastoma.Bioscience reports · 2020Article
- miR-96 Inhibits SV2C to Promote Depression-Like Behavior and Memory Disorders in Mice.Frontiers in behavioral neuroscience · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer, the second most common cancer in men, has been rarely explored by integrating mRNA and miRNA expression profiles. In this study, we combined two mRNA expression datasets and six documented miRNAs to uncover the comprehensive molecular mechanism of prostate cancer. Results showed that a total of 30 genes were significantly differentially expressed in 49 tumor samples by comparing with 22 normal samples. Importantly, all samples from the two datasets can be clearly classified into two groups, tumor group and normal group, based on the selected differentially expressed genes (DEGs). The miRNA-mRNA regulation network indicated that 4 out of 30 DEGs can be regulated by three miRNAs. In addition, prognostic performance validation using in silico databases showed that the DEGs can significantly differentiate between low-risk and high-risk prostate cancer. In summary, multiple biological processes are probably involved in the development and progression of prostate cancer. First, dysregulation of SV2 can regulate transporter and transmembrane transporter activity and then provide the necessary nutrients for tumor cell proliferation. Second, HOXD10 can induce cell proliferation via TCF-4. Finally, dysregulation of CACNA1D can further suppress tumor apoptosis in prostate cancer. The identification of critical genes and valuable biological processes can be useful for the understanding of the molecular mechanism of prostate cancer.
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Registered trials
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