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To investigate the effect of AMD1 gene expression on prostate cancer cells (PC-3M), explore the mechanism of AMD1 action in cancer cells, and examine the regulation of AMD1 gene expression by methionine (MET). Quantitative PCR (qPCR) and western blot analysis (WB) approaches were used to detect and measure gene expression. The cell apoptotic rate was determined by flow cytometric (FCM) analysis. qPCR and WB assays showed that both AMD1 gene expression and cell apoptotic rate were associated with MET. MET has a significant regulatory effect on the expression of the AMD1 gene and a certain amount of MET can promote the expression of the AMD1 gene. This provides a health guideline for a low-methionine diet for prostate cancer patients and scientific evidence for prostate cancer prevention. [ABSTRACT FROM AUTHOR]

Objective: The objective of this study was to investigate the involvement of the long non-coding RNA (lncRNA) BRE-AS1 in clear cell renal cell carcinoma (ccRCC) and to explore its potential therapeutic role., Methods: The expression of BRE-AS1 and miR-106b-5p was determined by qRT-PCR. Overexpression of BRE-AS1 and miR-106b-5p were performed to study their relationship. Transwell assays were used to evaluate cell movement. Methylation-specific PCR (MSP) was performed to explore the role of BRE-AS1 in the methylation of the miR-106b-5p gene., Results: The results showed that the expression levels of BRE-AS1 were decreased, while those of miR-106b-5p were increased in ccRCC tissues. BRE-AS1 was found to be closely associated with the prognosis of patients with ccRCC. The expression of BRE-AS1 was inversely correlated with that of miR-106b-5p in tumor tissues. Overexpression of BRE-AS1 led to decreased expression levels of miR-106b-5p and increased methylation of the miR-106b-5p gene, whereas miR-106b-5p did not affect the expression of BRE-AS1. BRE-AS1 inhibited the movement and proliferation of ccRCC cell lines, while miR-106b-5p suppressed the role of BRE-AS1., Conclusion: BRE-AS1 may suppress ccRCC by downregulating the expression of miR-106b-5p., (©The Author(s) 2024. Open Access. This article is licensed under a Creative Commons CC-BY International License.)

Background: Musashi1 (MSI1) has been reported to be involved in cancer development and progression. The biologic role of MSI1 in renal cell carcinoma (RCC), however, remains unknown., Methods: Expression of MSI1 in normal kidney cells and kidney cancer cells were measured by real-time PCR. In addition, MSI1 expression in 20 paired kidney cancer and non-cancerous tissues were quantified using real-time PCR. Furthermore, the expression of MSI1 in 115 kidney cancer samples was detected to analyze the correlations between MSI1 expression and the clinicopathological features of RCC patients. The biological function of MSI1 on tumor cell invasion and migration were explored through wound healing and transwell migration assays., Results: MSI1 was significantly upregulated in renal cancer cells and tissues compared with normal kidney cells and tissues. High levels of MSI1 were positively associated with tumor stage (P=0.002) and distant metastasis (P=0.013) of RCC patients. Patients with higher MSI1 expression had a significantly poorer overall and recurrence-free survival time (P=0.019 and P=0.012, respectively) than patients with low MSI1 expression. Multivariate analysis showed that MSI1 overexpression was an independent prognostic indicator (P=0.009 and P=0.015, respectively) for the survival of RCC patients. Ablation of MSI1 inhibited the invasion and metastasis of renal cancer cells., Conclusion: Our results suggest that MSI1 expression is upregulated in RCC, and that MSI1 plays an important role in promoting cell invasion and metastasis of RCC., Competing Interests: None., (IJCEP Copyright © 2019.)

Objective: The study aims to examine the effect of thymosin β10 (TMSB10) on renal cell carcinoma (RCC) progression and metastasis., Methods: Real-time PCR and immunohistochemistry analysis were used to evaluate TMSB10 expression in RCC tissue samples and renal cancer cells. Statistical analyses were applied to investigate the association between TMSB10 expression and the clinicopathological characteristics and prognosis of RCC patients. In vitro migration and invasion assays were performed in 786-O and ACHN cells., Results: The expression of TMSB10 was significantly higher in renal cancer cells and tissues compared with normal kidney cells and tissues. TMSB10 expression was significantly related to tumor stage (P=0.002), lymph node metastasis (P=0.034), and distant metastasis (P=0.039). Kaplan-Meier analysis suggested that high TMSB10 expression was significantly associated with unfavorable overall (P=0.004) and recurrent-free survival (P=0.025) of RCC patients. Furthermore, TMSB10 knockdown inhibited the migration and invasion abilities of renal cancer cells in vitro., Conclusion: TMSB10 is overexpressed in RCC and regulates malignant cell metastasis by inducing epithelial-mesenchymal transition, which makes TMSB10 a candidate therapeutic target for RCC., Competing Interests: None., (IJCEP Copyright © 2019.)