مقايسه بيان ژن‌هاي ARHGAP36 و IGSF1در بافت‌هاي سرطاني تيروئيد پاپيلاري و بافت‌هاي سالم مجاور آن در استان اصفهان، ايران

Papillary thyroid carcinoma (PTC) is the most preva‎lent endocrine malignancy yet its etiology remainsunclear., identifiying the genes involved in its development is therefore of significant importance. ARHGAP36 and IGSF1, two genes involved in the cellular signaling and intercellular interactions, respectively, may play crucial roles in PTC pathogenesis. This study aimed to compare the mRNA expression levels of ARHGAP36 and IGSF1 between PTC tumors and adjacent normal tissues. Microarray and RNA-seq data were collected from public databases for analysis. Additionally, clinical samples were collected from Sina Hospital (Isfahan) and analyzed using RT-qPCR. Statistical analyses were performed using REST2009, GraphPad Prism 10, and IBM SPSS Statistics 27 software. Both ARHGAP36 and IGSF1 were identified as differentially expressed genes between PTC tumors and adjacent normal tissues, based on microarray and RNA-seq data. The RT-qPCR results revealed that both genes were upregulated in the majority of PTC tumors; however, some tumors exhibited a lack of ARHGAP36 expression accompanied by decreased IGSF1 expression. The observed upregulation of these two genes and the lack of ARHGAP36 expression coupled with decreased IGSF1 expression in some tumors were further validated by a similar pattern of CDH1 expression changes. Increased expression of ARHGAP36 and IGSF1 was also observed in lymph node metastases. While no significant variation in ARHGAP36 expression was observed between metastatic and non-metastatic tumors, a considerable decrease in IGSF1 expression was identified in the metastatic tumors in comparison with the non-metastatic tumors. Furthermore, IGSF1 expression was higher in goiter tissues compared to adjacent normal tissues.These findings suggest that ARHGAP36 and IGSF1 may have dual roles in the initiation and progression of PTC, warranting further investigation to elucidate their molecular mechanisms.

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