Overexpression of MiR-155-5p and increased number of macrophage population in precancerous prostatic disease
Penulis/Author
Rachma Greta Perdana Putri (1); Sari Eka Pratiwi (2); dr. Didik Setyo Heriyanto, Sp.PA(K)., Ph.D (3); Dr. dr. R. Danarto, Sp.B., Sp.U(K). (4); dr. Indwiani Astuti Dr.Med. (5); dr. Nur Arfian, Ph.D. (6); Prof. dr. Sofia Mubarika Harjana, M.Med.Sc., Ph.D. (7)
Tanggal/Date
18 2020
Kata Kunci/Keyword
Abstrak/Abstract
Background
: Impaired microRNA(miR) regulation and chronic inflammation could transform tumors into
carcinoma and cancer by metastasis through cellular and genomic changes. Precancerous lesions have a
33.3 percent chance of becoming cancerous. This study investigated the role of miR-155 related to SOCS1
mRNA and macrophage population in disease progression associated with Benign Prostate Hyperplasia
(BPH), High-Grade Prostatic Intraepithelial Neoplasia (HGPIN), and Prostate Adenocarcinoma (PRAD).
Health Science Journal of Indonesia
Putri
et al.
86
Methods
: This was a cross-sectional study using three groups of samples, namely BPH, HGPIN, and
PRAD. Tissue samples were obtained from TURP Action. The expression of miR-155 was analyzed using
real-time qPCR and calculated using the Livak method. The expression of SOCS1 mRNA was analyzed
using reverse transcriptase PCR. The macrophage pan-marker, anti-CD68 monoclonal antibody (MoAb),
was used to detect macrophage population in tissues by immunohistochemistry
.
Results
: The expression of miR-155 was higher in HGPIN than BPH and PRAD (
p
=0.14). The expression
of SOCS1 mRNA in HGPIN was the lowest among the three samples (
p
=0.96). There was a negative
correlation between miR-155 and SOCS1 mRNA (
p
=0.02). There was a significant increase in the
percentage of the macrophage population in HGPIN (6.03 percent) compared to BPH (0.89 percent) with
p
=0.00.
Conclusion
: In this study, there were changes in the percentage of macrophage and miR-155 in HGPIN. The
variation in miR-155 expression and the percentage of the macrophage may be caused by epigenetic changes.
Therefore, further research is needed to validate these results and understand the possibility of being a biomarker
in precancerous disease of the prostate.
