ABSTRACT
Colorectal cancer (CRC) is one of the most frequently diagnosed cancers Worldwide, with rising incidence and mortality rates. Recent research has high-lighted the role of microRNAs (miRNAs) in regulating gene expression associated with tumor growth and progression. In a variety of malignancies, including CRC, it has been demonstrated that the tumor-suppressive miR-101-3p inhibits cancer cell invasion, proliferation, and metastasis.
Members of the ADAM (A Disintegrin and Metalloproteinase) family, including ADAM15, are transmembrane glycoproteins that are involved in angiogenesis, migration, and cell adhesion. They have also been linked to the development of cancer. Comparing CRC samples to nearby normal tissues, this study aimed to evaluate the expression levels of miR-101-3p and its predicted target gene, AD-AM15.
Formalin-fixed paraffin-embedded (FFPE) tissue specimens were obtained from 30 CRC patients at Zheen International Hospital. For each case, matched pairs of cancerous and surrounding non-cancerous tissues were collected. Total RNA was extracted from all specimens and converted into cDNA for downstream quantita-tive analysis.
The expression levels of miR-101-3p and ADAM15 were determined using quan-titative real-time PCR (qRT-PCR). The housekeeping gene β-actin was employed as an internal control. Expression data were examined using the relative gene ex-pression method (Livak method) to estimate relative fold changes between tu-mor and non-tumor tissues.
The results demonstrated a significant downregulation of miR-101-3p in colorec-tal tumor tissues compared to adjacent normal tissues, with a mean fold change of 0.26, representing an approximate 74% reduction in expression. In contrast, ADAM15 expression was significantly upregulated in tumor tissues, showing a mean fold change of 2.82, corresponding to an approximate 182% increase rela-tive to controls. A statistical analysis revealed a negative association between the expression levels of these two molecules, indicating that miR-101-3p might function as a negative regulator of ADAM15.
To our knowledge, this study represents the first analysis of the relationship be-tween miR-101-3p and ADAM15 in CRC cases in the Kurdistan Region. The find-ings support the hypothesis that reduced miR-101-3p expression may contribute to CRC progression via ADAM15 deregulation. These data suggest that miR-101-3p and ADAM15 could be indicators for CRC diagnosis or prognosis, as well as prospective treatment targets.
This study provides new insights into the molecular landscape of CRC and under-scores the importance of investigating miRNA-mediated gene regulation in can-cer pathogenesis
