Affiliation:
1. Ahvaz Jundishapur University of Medical Sciences: Ahvaz Jondishapour University of Medical Sciences
2. Shahid Beheshti University of Medical Sciences School of Medicine
3. Zabol University of Medical Sciences
4. Shahid Beheshti University of Medical Sciences Research Institute for Gastroenterology and Liver Diseases
5. Tehran University of Medical Sciences
Abstract
Abstract
Background: Aberrant activation of Wnt pathway is linked to dysregulation of several genes. DACT1 and DACT2 are members of the DACT family that participate in antagonizing of the Wnt signaling cascade. Thus in this study we assess the mRNA levels of DACT1, DACT2 and Cyclin D1 in CRC tissues compared to adjacent tissues.
Methods: Determination of the mRNA levels of DACT1, DACT2and Cyclin D1 was done by Quantitative Real-Time PCR (qRT-PCR). The correlation between DACT1, DACT2 and Cyclin D1 genes was examined. Receiver operating characteristic (ROC) curves was plotted to assess the diagnostic power. The association between histopathological parameters and the DACT1, DACT2 and Cyclin D1 gene was investigated.
Results: The levels of DACT1 and Cyclin D1 were remarkably higher in CRC tissue than adjacent tissues (P<0.0001). However, the expression of DACT2 was decreased (P<0.001). Between DACT1 and Cyclin D1 expression levels have a positive correlated (P<0.0001). DACT1 (AUC = 0.74, P<0.0001), DACT2 (AUC = 0.69, P<0.0003) and Cyclin D1 (AUC = 0.75, P<0.0001) had good effectiveness in separation between CRC samples and control. We found a significant association between DACT1 expression with tumor site (P <0.01). Also, a significant association was detected between DACT2 and Cyclin D1 with tumor stage (P <0.005 and P <0.038 respectively).
Conclusion: The findings suggested that DACT1 could function as an oncogene and correlation of DACT1 with Cyclin D1 expression suggests that DACT1expression is related to CRC progression whereas DACT2 was frequently downregulated and can be considered as a tumor suppressor.
Publisher
Research Square Platform LLC
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