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Updated: Jun 1, 2026

MicroRNA Detection in Prostate Tumors by Quantitative Real-time PCR (qPCR)
Published on: May 16, 2012
Downregulation of Sec23A protein by miRNA-375 in prostate carcinoma
Jaroslaw Szczyrba1, Elke Nolte, Sven Wach
1Institut für Medizinische Mikrobiologie und Hygiene, Abteilung Virologie, Haus 47, Universitätsklinikum, 66421 Homburg/Saar, Germany.
Abstract:
Prostate carcinoma (CaP) is a leading cause of cancer-related death in men. We have previously determined the microRNA (miRNA) profile of primary CaP in comparison with nontumor prostate tissue. miRNAs are small, noncoding RNAs that inhibit protein synthesis on a posttranscriptional level by binding to the 3'-untranslated region (3'-UTR) of their target genes. In primary CaP tissue, we have previously found by miRNA sequencing that miR-375 and miR-200c were upregulated 9.1- and 4.5-fold, respectively. A computational analysis predicted the 3'-UTR of the SEC23A gene as a potential target for both miR-375 and miR-200c. Here, we show that the 3'-UTR of SEC23A mRNA is indeed a target for miR-375 and miR-200c and that both miRNAs downregulate Sec23A protein expression when ectopically expressed in human 293T cells. In primary samples of CaP, we found a direct correlation between reduction of SEC23A mRNA and overexpression of miR-375 but not of miR-200c. The reduced levels of Sec23A protein were inversely correlated to the increased amount of miR-375 in the LNCaP and DU145 CaP cell lines when compared with normal prostate fibroblasts. In primary CaP, we also detected decreased amounts of Sec23A protein when compared with corresponding normal prostate tissue. Ectopically overexpressed Sec23A in LNCaP and DU145 CaP cells significantly reduced the growth properties, indicating that Sec23A might play a role in the induction or growth of prostate carcinoma. Sec23A overexpression reduced cell growth but did not induce apoptosis, whereas inhibition of Sec23A stimulated cell proliferation.
Insights
MicroRNAs miR-375 and miR-200c target SEC23A in prostate cancer. Overexpression of miR-375 correlates with reduced SEC23A, impacting cancer cell growth.
Area of Science:
- Oncology
- Molecular Biology
- Genetics
Background:
- Prostate carcinoma (CaP) is a significant cause of cancer-related mortality in men.
- MicroRNAs (miRNAs) are key regulators of gene expression, influencing various cellular processes.
- Previous studies identified altered miRNA profiles in primary CaP.
Purpose of the Study:
- To investigate the regulatory role of miR-375 and miR-200c on SEC23A in prostate cancer.
- To determine the correlation between SEC23A expression and specific miRNAs in CaP.
- To evaluate the impact of Sec23A on prostate cancer cell growth.
Main Methods:
- miRNA sequencing and computational analysis to identify potential miRNA targets.
- Validation of SEC23A as a target for miR-375 and miR-200c using cell-based assays.
- Correlation analysis of miRNA and SEC23A mRNA/protein levels in CaP tissues and cell lines.
- Assessment of Sec23A's effect on CaP cell proliferation and apoptosis.
Main Results:
- The 3'-untranslated region (3'-UTR) of SEC23A mRNA was confirmed as a target for miR-375 and miR-200c.
- Both miRNAs were found to downregulate Sec23A protein expression.
- A negative correlation was observed between miR-375 and SEC23A mRNA in primary CaP.
- Reduced Sec23A protein levels were inversely correlated with increased miR-375 in CaP cell lines and tissues.
- Overexpression of Sec23A inhibited CaP cell growth, while its inhibition stimulated proliferation.
Conclusions:
- miR-375 and miR-200c directly target SEC23A, downregulating its protein expression in prostate cancer.
- miR-375's upregulation is associated with decreased SEC23A levels in CaP.
- Sec23A plays a role in regulating prostate cancer cell proliferation, suggesting its potential as a therapeutic target.
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