Title of article :
No Association Between Expression of RAS Guanyl Releasing Protein 3 (RASGRP3) in Breast Cancer and Clinicopathological Data
Author/Authors :
Shams, Roshanak Department of Medical Genetics - Shahid Beheshti University of Medical Sciences, Tehran, Iran , Ghafouri-Fard, Soudeh Department of Medical Genetics - Shahid Beheshti University of Medical Sciences, Tehran, Iran
Pages :
3
From page :
1
To page :
3
Abstract :
Over-activation of Ras signaling pathway is implicated in the pathogenesis of several malignancies including breast cancer. Ras Guanyl nucleotide releasing peptides (RasGRPs) are a group of Ras guanine nucleotide exchange factors (RasGEFs), which participate in the activation of Ras signaling pathway. The RasGRP3 induces the expression and function of H-Ras and R-Ras proteins and plays oncogenic roles in numerous malignancies (1). Overexpression of RasGRP3 protein has been demonstrated in human breast tumor tissue samples compared with normal breast samples. Its silencing in breast cancer cells has diminished cell proliferation, triggered apoptosis in MCF7 cells, and made T-47D cells responsive to Tamoxifen and trastuzumab (1). On the other hand, RASGRP3 has been predicted to be a target of miR-100 regulatory function (2) a miRNA, whose participation in breast cancer pathogenesis has been highlighted (3). In order to find the clinical relevance of RASGRP3 expression in breast cancer patients, we evaluated RASGRP3 expression in 50 invasive ductal carcinomasamples compared with the corresponding adjacent non-cancerous tissues (ANCTs) by means of quantitative real time PCR after receiving the approval of Ethics Committee of Shahid Beheshti University of Medical Sciences (IR.SBMU. MSP.REC.1396.451) and obtaining informed consents from all patients. All patients were sporadic cases of breast cancer and had no history of radio/chemotherapy.
Keywords :
RAS Guanyl Releasing Protein , Breast Cancer , Clinicopathological Data
Journal title :
Astroparticle Physics
Serial Year :
2018
Record number :
2482466
Link To Document :
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