Background: Prostate cancer (PCa) is one of the most prevalent cancers that occur in men worldwide. Autophagyrelated genes (ARGs) may play an essential role in multiple biological processes of prostate cancer. However, ARGs expression signature has rarely been used to investigate the association between autophagy and prognosis in PCa. This study aimed to identify and assess prognostic ARGs signature to predict overall survival (OS) and disease-free survival (DFS) in PCa patients. Methods: First, a total of 234 autophagy-related genes were obtained from The Human Autophagy Database. Then, differentially expressed ARGs were identified in prostate cancer patients based on The Cancer Genome Atlas (TCGA) database. The univariate and multivariate Cox regression analysis was performed to screen hub prognostic ARGs for overall survival and disease-free survival, and the prognostic model was constructed. Finally, the correlation between the prognostic model and clinicopathological parameters was further analyzed, including age, T status, N status, and Gleason score. Results: The OS-related prognostic model was constructed based on the five ARGs (FAM215A, FDD, MYC, RHEB, and ATG16L1) and significantly stratified prostate cancer patients into high-and low-risk groups in terms of OS (HR = 6.391, 95% CI = 1.581-25.840, P < 0.001). The area under the receiver operating characteristic curve (AUC) of the prediction model was 0.84. The OS-related prediction model values were higher in T3-4 than in T1-2 (P = 0.008), and higher in Gleason score > 7 than ≤ 7 (P = 0.015). In addition, the DFS-related prognostic model was constructed based on the 22 ARGs (ULK2,
Increasing evidence indicates that long non-coding RNAs (lncRNAs) have been associated with cancer development. However, the contributions of lncRNAs to renal cell carcinoma (RCC) remain poorly characterized. Here, we identified a novel lncRNA, termed HEIRCC, which was up-regulated in RCC tissues through lncRNA microarray analysis and subsequent validation in 60 RCC clinical specimens and cell lines. The high expression of HEIRCC is associated closely with the clinical pathology features such as larger tumor size, poor differentiation, lymphatic metastasis. In vitro assays revealed that HEIRCC knockdown could inhibit cell proliferation, trigger late apoptosis, suppress cell migration and invasion. We further demonstrated that depletion of HEIRCC reduce the epithelial to mesenchymal transition (EMT) program by regulating expression levels of EMT-associated markers in RCC cells. Thus, HEIRCC might be act as an important regulator of EMT in RCC progression and might be a novel therapeutic target for the advanced RCC therapy.
To clarify the mechanism of circGOLPH3 regulation on prostate cancer cells, we performed an over-expression and interference circGOLPH3 assay in prostate cancer cells PC-3 and then evaluated cellular viability, proliferation, cell cycle, and apoptosis of prostate cancer cells by MTT, CCK8, Edu stain, TUNEL stain, and flow cytometry. Binding proteins of CircGOLPH3 were identified by RNA pull-down, mass spectrometry, and RNA-binding protein immunoprecipitation (RIP) assays. The expressions of CircGOLPH3 and CBX7 were measured by qRT-PCR. The results showed that after over-expression of circGOLPH3, the proliferative capacity and the viability of PC-3cells were significantly improved, whereas apoptosis was inhibited. CircGOLPH3 could bind to the CBX7 protein that was highly expressed in the PC-3 cell. Additionally, a functional test on CBX7 showed that the CBX7 over-expression notably improved the proliferative capacity and the viability of PC-3 cells and decreased cellular apoptosis, which was consistent with the effects of circGOLPH3. The validated this study that circGOLPH3 and its binding protein CBX7can promote prostate cancer cell proliferation and inhibit apoptosis.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.