Research Article - Biomedical Research (2017) Volume 28, Issue 14
Analysis of the expression of autophagy-related protein in prostate cancer and preliminary investigation of its clinical significance
Objective: To analyze the differences in the expression of Autophagy-related proteins (ATG) in prostate cancer tissues and normal para-carcinoma tissues and to have a preliminary investigation of its clinical significance.
Methods: The 90 cases of specimens from the prostate cancer radical operation without the endocrinotherapy from Jan 2013 to Dec 2015 were collected by means of the immunohistochemical staining, the immunohistochemical staining results of the following 8 antibodies in the prostate cancer tissues and normal para-carcinoma tissues were observed: Androgen Receptor (AR), phosphomammalian Target of Rapamycin (p-mTOR), Beclin-1, Autophagy-related protein5 (ATG5), Autophagyrelated protein7 (ATG7), ULK1, p62 and microtubule-associated protein light chain 3B (LC3B). Two pathologists performed the scoring independently according to the same scoring criteria and made a comparative statistical analysis in accordance with the scoring results.
Results: The immunohistochemical staining results showed that, the expression of autophagy-related protein p62 (t=2.189, P=0.048), p-mTOR (t=3.956, P<0.001) and AR (t=4.954, P<0.001) in the prostate cancer tissues were significantly up-regulated when compared with the normal para-carcinoma prostate tissues, and the expression of Beclin1 (t=2.855, P=0.005) and ULK1 (t=5.098, P<0.001) was significantly down-regulated when compared with the normal tissues. The difference among ATG5 (t=1.110, P=0.269), ATG7 (t=1.396, P=0.164) and LC3B (t=1.667, P=0.097) in terms of the expression level was of no statistical significance.
Conclusion: Cellular autophagy is inhibited in prostate cancer tissues and with the increase in tumor grade and staging, the inhibition degree of cellular autophagy will also escalate, but the specific mechanism is still needed to further investigate.Author(s): Lunfeng Zhu, Xiaolin Deng, Hua Chen, Rui Liu, Jinxiang Luo, Guanghua Peng