Bioinformatic study on the role of PI3K/AKT pathway and LncRNAs in Prostate Cancer
Bioinformatic study on the role of PI3K/AKT pathway and LncRNAs in Prostate Cancer
Yasaman Shafiei,1Mansoureh Azadeh,2,*Pegah Javid,3Behshid Hooshangi,4Melika Mazaheri Tehrani,5
1. Zist Fanavari Novin Biotechnology Department 2. Zist Fanavari Novin Biotechnology Department 3. Zist Fanavari Novin Biotechnology Department 4. Zist Fanavari Novin Biotechnology Department 5. Zist Fanavari Novin Biotechnology Department
Introduction: Prostate cancer is the most frequent cancer in men. Aging process, ethnicity, and genetic factors are three recognized risk factors for PCa. The state of tumor differentiation is highly correlated with a group of genes that have been discovered. The phosphatidylinositol 3-kinase (PI3K)/AKT pathway plays an important role in PCa carcinogenesis, according to a huge amount of evidence.
Methods: To achieve this goal, GEO data base and KEGG pathways were used to gain information about PI3K/AKT pathway and LncRNADisease data base was studied to choose lncRNAs associated with prostate cancer. The result showed that SCHLAP1 with Score: 0.9989 is linked to PCa.
Results: PI3K/AKT pathway result in apoptosis and proliferation of PCa cells and tumor metastasis and invasion by regulating several pathways. PI3K/AKT pathway is stimulated by The CCR9-CCL25 axis and IL-6, giving rise to PCa cell apoptosis resistance. IGF-I/PI3K/Akt signaling can lead to activating androgen receptor (AR), resulting in cell proliferation. Inactivation of PTEN can negatively activate AKT and mTOR. The aim of this study is to find the rule of PI3K/AKT pathway in the process of prostate cancer. We identified high SChLAP1 expression as significantly prognostic for metastatic disease progression of prostate cancer.
Conclusion: Based on the studies, it is concluded that PI3K/AKT signaling plays a significant role in PCa tumorigenesis. The mechanisms of PI3K/AKT in PCa tumorigenesis are multiple; inflammation, cell cycling, and angiogenesis are involved in this signaling. In additional we characterize a lncRNA termed SChLAP1overexpressed in a subset of prostate cancers.