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BAP1 serves as a clear-cell renal cell carcinoma suppressor and is inversely regulated by miR-200c-3p

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Abstract The initiation and development of malignant tumor is always accompanied by a series of complex gene expression alterations inside the cells. As a tumor suppressor, the deubiquitinating enzyme BAP1 has been identified as an important regulator on the outcomes and biological properties of clear-cell renal cell carcinoma (ccRCC). However, BAP1-involved intracellular regulatory cascades in clear-cell renal cell carcinoma are still not fully understood. In this study, we provided evidence that the protein levels of BAP1 were dramatically diminished in clear-cell renal cell carcinoma in vitro and in vivo. Notably, the relatively low expression of BAP1 is significantly associated with worse prognosis in ccRCC patients. Besides, through the prediction of bioinformatics methods and verification of biological experiments, we confirmed that miR-200c-3p was the direct upstream regulator of BAP1. Taken together, our study presents an important role of miR-200c-3p/BAP1 in the development of ccRCC, which provided an alternative strategy for treating ccRCC in clinical practice.
Title: BAP1 serves as a clear-cell renal cell carcinoma suppressor and is inversely regulated by miR-200c-3p
Description:
Abstract The initiation and development of malignant tumor is always accompanied by a series of complex gene expression alterations inside the cells.
As a tumor suppressor, the deubiquitinating enzyme BAP1 has been identified as an important regulator on the outcomes and biological properties of clear-cell renal cell carcinoma (ccRCC).
However, BAP1-involved intracellular regulatory cascades in clear-cell renal cell carcinoma are still not fully understood.
In this study, we provided evidence that the protein levels of BAP1 were dramatically diminished in clear-cell renal cell carcinoma in vitro and in vivo.
Notably, the relatively low expression of BAP1 is significantly associated with worse prognosis in ccRCC patients.
Besides, through the prediction of bioinformatics methods and verification of biological experiments, we confirmed that miR-200c-3p was the direct upstream regulator of BAP1.
Taken together, our study presents an important role of miR-200c-3p/BAP1 in the development of ccRCC, which provided an alternative strategy for treating ccRCC in clinical practice.

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