بررسی کمی بیان ژن Bid در نمونه بیوپسی پولیپ‌های آدنوماتوز روده بزرگ

Background: Most of colorectal cancers arise from intestinal polyps. Evaluating of the expression level of genes that are involved in tumors growth and development, may consider as diagnostic factor of malignancy in the polyps. Failure of apoptosis is one of the causes of cancers. One of the key molecules in this pathway is Bid gene which connects the extrinsic to the intrinsic apoptosis pathways. The aim of this study was to investigate the quantitative expression of Bid gene in colorectal adenomatous polyps compared to control group. Methods: The investigated population was chosen from the cases with colonic polyps that referred to the Taleghani Hospital, Tehran, Iran, from April 2014 to May 2016. 22 biopsy samples from patients with adenomatous polyps and 10 samples from healthy individuals as control group were selected. Demographic and clinical properties were collected from patients' files. The Bid gene expression was evaluated using Real-time PCR by ABI 7500 (Applied Biosystems Inc., Foster City, CA, USA). Results were analyzed by the ABI 7500 system SDS version 2.3 and GraphPad Prism, version 5 (GraphPad Software Inc., La Jolla, CA, USA). the expression changes of the intended gene in target groups were compared with the normal tissues using the 2-∆∆CT equation. Results: Based on the quantitative real-time PCR, the gene expression of Bid gene significantly increased in adenomatous polyps in comparison with the control group (healthy individuals) (RQ>2). Also, polyps were seen in ascending colon, transverse colon, descending colon and rectum showed increased expression compared to control group, but in the sigmoid section of the intestine, there was no change in expression of Bid gene compared to control group. Conclusion: According to the present study, the expression of Bid gene increased in adenomatous polyps, compared with the normal tissue (healthy group). It suggests that Bid gene by increasing the expression in response to the onset of dysplasia and disruption of the apoptotic cycle, it tries to compensate for the apoptosis.