ArticleMolecular medicine reports2018
Exploration of the diagnostic value and molecular mechanism of miR‑1 in prostate cancer: A study based on meta‑analyses and bioinformatics.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- Innovative molecular targets for combatting metastasis in adrenocortical carcinoma.Frontiers in endocrinology · 2025Article
- Article
- Article
- The Role of Androgen Receptor and microRNA Interactions in Androgen-Dependent Diseases.International journal of molecular sciences · 2022Review
- Downregulation of MicroRNA-1 and Its Potential Molecular Mechanism in Nasopharyngeal Cancer: An Investigation Combined with In Silico and In-House Immunohistochemistry Validation.Disease markers · 2022Article
- The Comprehensive Analysis of Hub Gene ARRB2 in Prostate Cancer.Disease markers · 2022Article
- Down-regulation of microRNA-125b-2-3p is a risk factor for a poor prognosis in hepatocellular carcinoma.Bioengineered · 2021Article
- Proliferating cell nuclear antigen clamp associated factor, a potential proto-oncogene with increased expression in malignant gastrointestinal tumors.World journal of gastrointestinal oncology · 2021Review
- CASC11 promotes aggressiveness of prostate cancer cells through miR-145/IGF1R axis.Prostate cancer and prostatic diseases · 2021Article
- Identification of Key MicroRNAs and Mechanisms in Prostate Cancer Evolution Based on Biomarker Prioritization Model and Carcinogenic Survey.Frontiers in genetics · 2020Article
- Identification of key genes and long non-coding RNA associated ceRNA networks in hepatocellular carcinoma.PeerJ · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prostate cancer (PCa) remains a principal issue to be addressed in male cancer‑associated mortality. Therefore, the present study aimed to examine the clinical value and associated molecular mechanism of microRNA (miR)‑1 in PCa. A meta‑analysis was conducted to evaluate the diagnosis of miR‑1 in PCa via Gene Expression Omnibus and ArrayExpress datasets, The Cancer Genome Atlas miR‑1 expression data and published literature. It was identified that expression of miR‑1 was significantly downregulated in PCa. Decreased miR‑1 expression possessed moderate diagnostic value, with area under the curve, sensitivity, specificity and odds ratio values at 0.73, 0.77, 0.57 and 4.60, respectively. Using bioinformatics methods, it was revealed that a number of pathways, including the 'androgen receptor signaling pathway', 'androgen receptor activity', 'transcription factor binding' and 'protein processing in the endoplasmic reticulum', were important in PCa. A total of seven hub genes, including phosphoribosylaminoimidazole carboxylase and phosphoribosylaminoimidazolesuccinocarboxamide synthase (PAICS), cadherin 1 (CDH1), SRC proto‑oncogene, non‑receptor tyrosine kinase, twist family bHLH transcription factor 1 (TWIST1), ZW10 interacting kinetochore protein (ZWINT), PCNA clamp associated factor (KIAA0101) and androgen receptor, among which, five (PAICS, CDH1, TWIST1, ZWINT and KIAA0101) were significantly upregulated and negatively correlated with miR‑1, were identified as key miR‑1 target genes in PCa. Additionally, it was investigated whether miR‑1 and its hub genes were associated with clinical features, including age, tumor status, residual tumor, lymph node metastasis, pathological T stage and prostate specific antigen level. Collectively the results suggest that miR‑1 may be involved in the progression of PCa, and consequently be a promising diagnostic marker. The 'androgen receptor signaling pathway', 'androgen receptor activity', 'transcription factor binding' and 'protein processing in the endoplasmic reticulum' may be crucial interactive pathways in PCa. Furthermore, PAICS, CDH1, TWIST1, ZWINT and KIAA0101 may serve as crucial miR‑1 target genes in PCa.
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