Background <p>The pathogenesis of CRC requires primary genetic and epigenetic mechanisms including, methylation of CpG islands of the genes. In the current study, micro RNA-139-5p (<i>miR</i>-139-5p) promoter methylated DNA was evaluated in tumor tissue and plasma samples from CRC affected patients.</p> Methods <p><i>MiR</i>-139-5p promoter methylation was investigated in 80 samples of tumoral tissue and healthy marginal tissue and the same number of plasma samples, using the MethyLight method. The miR-139-5p expression was assessed using the qPCR method. BT (Bioassay Technology) Elisa kit was applied to measure RAP-1b as a target gene of miR-139-5p.</p> Results <p>Median PMR values of 12.4 (95% CI, 3.23–32.25) and 0.66 (95%CI, 0.51–1.0) were obtained from plasma samples of CRC patients and controls, sequentially. In plasma samples, the sensitivity and specificity of <i>miR</i>-139-5p promoter methylated marker were 75% and 92.5%, in the same order (AUC = 0.958).</p> <p>Lower expression of miR-139-5p in plasma and tumor tissue of patients (<i>P</i> &lt; 0.001) was shown. Also, a significant rise of RAP-1b protein concentration was observed in both mentioned specimens.</p> Conclusion <p>Hyper-methylation of <i>miR</i>-139-5p could be suggested as high accuracy diagnostic biomarker for the detection of CRC in plasma samples, pending further validation with large prospective studies.</p>

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Evaluation of epigenetic silencing of the miR-139-5p gene in the pathogenesis of colorectal cancer and its diagnostic biomarker capability in plasma samples

  • Masoud Asefi,
  • Nayebali Rezvani,
  • Massoud Saidijam,
  • Ali Reza Soltanian,
  • Ali Reza Khalilian,
  • Ali Mahdavinezhad

摘要

Background

The pathogenesis of CRC requires primary genetic and epigenetic mechanisms including, methylation of CpG islands of the genes. In the current study, micro RNA-139-5p (miR-139-5p) promoter methylated DNA was evaluated in tumor tissue and plasma samples from CRC affected patients.

Methods

MiR-139-5p promoter methylation was investigated in 80 samples of tumoral tissue and healthy marginal tissue and the same number of plasma samples, using the MethyLight method. The miR-139-5p expression was assessed using the qPCR method. BT (Bioassay Technology) Elisa kit was applied to measure RAP-1b as a target gene of miR-139-5p.

Results

Median PMR values of 12.4 (95% CI, 3.23–32.25) and 0.66 (95%CI, 0.51–1.0) were obtained from plasma samples of CRC patients and controls, sequentially. In plasma samples, the sensitivity and specificity of miR-139-5p promoter methylated marker were 75% and 92.5%, in the same order (AUC = 0.958).

Lower expression of miR-139-5p in plasma and tumor tissue of patients (P < 0.001) was shown. Also, a significant rise of RAP-1b protein concentration was observed in both mentioned specimens.

Conclusion

Hyper-methylation of miR-139-5p could be suggested as high accuracy diagnostic biomarker for the detection of CRC in plasma samples, pending further validation with large prospective studies.