Abstract
Background The role of miRNAs in renal cell carcinoma (RCC) is not certain. We wanted to study the biological functions and potential mechanisms of miR-101-3p in RCC. Methods miR-101-3p was inhibited in A498 and OSRC-2 (two RCC cell lines). We studied its effect on cell invasion and proliferation. Target EZH2 of miR-101-3p was designated by different methods, including luciferase functional analysis and Western blotting. The expression level of the target gene in treated cells was quantitatively analyzed by quantitative real-time polymerase chain reaction. In addition, induction of miR-101-3p to prevent tumor formation of A498 cells in mice was further studied. Results The overexpression of miR-101-3p significantly inhibited the proliferation, migration, and invasion in two RCC cells. Western blotting and luciferase functional analysis indicated that miR-101-3p regulated the expression of EZH2 in two cell lines. Mice inoculated with A498 and OSRC-2 cells transfected with miR-101-3p mimics showed significantly smaller xenografts and weaker EZH2 expression levels than the control group. Conclusions miR-101-3p inhibited RCC cell proliferation, migration, and invasion by targeting EZH2.
Highlights
renal cell carcinoma (RCC) is one of the most common malignancies of the urinary system [1], accounting for about 2%~3% of adult malignancies [2]
Based on the starBase database, we found overexpression of miR-101-3p in RCC tissues compared with normal samples (P < 0:01), and Kaplan-Meier survival analysis revealed that high expression of miR-101-3p was closely associated with poor survival (P < 0:005) (Figure 1(c))
In RCC cells, these results reported that EZH2 exerted tumor effects with miR-101-3p
Summary
We wanted to study the biological functions and potential mechanisms of miR-101-3p in RCC. MiR-101-3p was inhibited in A498 and OSRC-2 (two RCC cell lines). We studied its effect on cell invasion and proliferation. Target EZH2 of miR-101-3p was designated by different methods, including luciferase functional analysis and Western blotting. Induction of miR-101-3p to prevent tumor formation of A498 cells in mice was further studied. The overexpression of miR-101-3p significantly inhibited the proliferation, migration, and invasion in two RCC cells. Western blotting and luciferase functional analysis indicated that miR-101-3p regulated the expression of EZH2 in two cell lines. Mice inoculated with A498 and OSRC-2 cells transfected with miR-101-3p mimics showed significantly smaller xenografts and weaker EZH2 expression levels than the control group. MiR-101-3p inhibited RCC cell proliferation, migration, and invasion by targeting EZH2 Conclusions. miR-101-3p inhibited RCC cell proliferation, migration, and invasion by targeting EZH2
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