Affiliations: [a] Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran | [b] Department of Surgery, Sina Hospital, Tehran University of Medical Sciences, Tehran, Iran | [c] Department of Molecular Medicine, School of Advanced Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran
Correspondence:
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Corresponding author: Soudeh Ghafouri-Fard, Department of Medical Genetics, Shahid Beheshti University of Medical Sciences, Tehran, Iran. E-mail: s.ghafourifard@sbmu.ac.ir.
Abstract: Long non-coding RNAs (lncRNA) constitute a significant percentage of RNAs with no translation to proteins. Their participation in fundamental aspects of cell physiology as well as their dysregulation in a number of pathologic conditions such as cancer have been documented. Among lncRNAs is actin filament associated protein 1 antisense RNA1 (AFAP1-AS1) whose elevated expression levels have been demonstrated in different cancers. In the in the present study we evaluated expression levels of AFAP1-AS1 and its antisense protein coding gene AFAP1 in breast cancer samples compare with adjacent non-cancerous tissues (ANCTs) as well as breast cancer cell lines with special focus on the assessment of the association between their transcript levels and patients’ clinicopathological data. AFAP1-AS1 has shown significant up-regulation in both MDA-MB-231 and MCF-7 compared with control sample. AFAP1-AS1 has been shown to be expressed in all of tumor tissues but 76% (39 out of 51) ANCTs. AFAP1 expression was not significantly different between tumor samples and ANCTs. AFAP1-AS1 has been demonstrated to be significantly up-regulated in tumor tissues compared with ANCTs (fold change = 4.65, P= 0.028). No significant correlation has been detected between the levels of these two transcripts in tumor tissues (R=2 0.081) or ANCTs (R=2 0.115). No significant associations have been found between expression levels of these genes and patients’ characteristics. However, both genes were significantly down-regulated in Ki-67 negative tumor samples. The observed up-regulation of AFAP1-AS1 in tumor samples compared with ANCTs implies its involvement in breast cancer pathogenesis and potentiates it as a biomarker or therapeutic target.
