As a member of the L1 family of neural cell molecules, close homologue of L1 (CHL1) has been proved to be downregulated in several human cancers. In the present study, we aimed to assess the expression and prognostic value of CHL1 in clear cell renal cell carcinoma (CCRCC). Immunohistochemistry was performed to detect the expression of CHL1 in tissue microarray chips. Then we compared specific clinicopathologic features in patients with different CHL1 expressions. The correlation between CHL1 expression and overall survival (OS) was evaluated by the Kaplan-Meier method and Cox regression analysis. We found that the expression of CHL1 was significantly lower in CCRCC tissues compared with adjacent normal tissues, which was correlated with TNM stage (P < 0.001), Fuhrman grade (P = 0.006), and LVI (P = 0.004). The Kaplan-Meier survival analysis indicated that CCRCC patients with low CHL1 expression had a poorer OS rate than those with high CHL1 expression (P < 0.001). Univariate and multivariate Cox regression analyses suggested that CHL1 was an independent and unfavorable prognostic factor for the OS rate of CCRCC patients. Collectively, low expression of CHL1 might predict poor OS rate of CCRCC.
Background Colorectal cancer is the third most common malignant tumor in the world and the fourth most common cancer-related death cause. Previous studies have confirmed that miR-183-5P is considered to be a cancer-associated miRNA in several tumor types. Methods We analyzed the expression of miR-183-5P in cancer tissues and adjacent tissues in TCGA database. The expression of miR-183-5P and QKI-5 mRNA was measured by RT-qPCR and western blot. CCK-8 were used to indicate the proliferation capacity. BALB/c nude mice were used to simulate in vivo experiments. Results In this study, we identified miR-183-5p as a tumor promoter in colorectal cancer. The expression of miR-183-5p was found upregulated in human colorectal cancer tissues while QKI-5 was down-regulated. CCK-8 assay demonstrated that miR-183-5p promoted colorectal cancer cell proliferation. We also found miR183-5P can target QKI-5 and inhibit its expression in CRC cell lines. Restoration of QKI-5 reversed the effects of miR-183-5p in colorectal cancer cells. Conclusion Taken together, our results suggest that miR-183-5p might function as a tumor-promoting factor in colorectal cancer and might contribute to its proliferation.
Background: Prostate cancer (PCa) is one of the common malignant tumors and it is difficult to diagnose at its early stage. MiR-183-5p has been reported involved in the proliferation of human PCa, this study aimed to investigate how miR-183-5p affects the migration and invasion of prostate cancer. Methods: In this study, we analyzed the expression of miR-183-5p in PCa patients and its correlation with clinicopathological parameters based on TCGA data portal. CCK-8, migration assay and invasion and wound-healing assay were performed to detect proliferation, migration and invasion in PCa cells. Results:We found the expression of miR-183-5p was significantly increased in PCa tissues, and high expression of miR-183 was positively associated with poor prognosis of PCa patients. Over-expression of miR-183-5p promoted the migration, invasion capacities of PCa cells, whereas knockdown of miR-183-5p showed reversed function. Furthermore, luciferase reporter assay showed TET1 was identified as a direct target of miR-183-5p, which was negatively correlation with miR-183-5p expression level. Importantly, rescue experiments demonstrated TET1 over-expression could reverse miR-183-5p mimic induced-acceleration of PCa malignant progression. Conclusion:Our results indicated that miR-183-5p could act as a tumor promoter in PCa and it accelerated the malignant progression of PCa by directly targeting and down-regulating TET1.
Background Prostate cancer (PCa) is one of the common malignant tumors worldwide. MiR-183-5p has been reported involved in the initiation of human PCa, this study aimed to investigate whether miR-183-5p affects the development of prostate cancer. Methods In this study, we analyzed the expression of miR-183-5p in PCa patients and its correlation with clinicopathological parameters based on TCGA data portal. CCK-8, migration assay and invasion and wound-healing assay were performed to detect proliferation, migration and invasion in PCa cells. Results We found the expression of miR-183-5p was significantly increased in PCa tissues, and high expression of miR-183 was positively associated with poor prognosis of PCa patients. Over-expression of miR-183-5p promoted the migration, invasion capacities of PCa cells, whereas knockdown of miR-183-5p showed reversed function. Furthermore, luciferase reporter assay showed TET1 was identified as a direct target of miR-183-5p, which was negatively correlation with miR-183-5p expression level. Importantly, rescue experiments demonstrated TET1 over-expression could reverse miR-183-5p mimic induced-acceleration of PCa malignant progression. Conclusion Our results indicated that miR-183-5p could act as a tumor promoter in PCa and it accelerated the malignant progression of PCa by directly targeting and down-regulating TET1.
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