Zinc Finger Protein 36 Triggers Proliferation in Renal Cell Carcinoma by Negatively Regulating Krüppel-Like Transcription Factor 10

Abstract

To uncover the role of Zinc finger protein 36 (Zfp36) in aggravating the development of renal cell carcinoma (RCC) and its regulatory effects on Krüppel-like transcription factor 10 (KLF10). Differential expressions of Zfp36 in 50 RCC tissues and their paracancerous ones were detected. Zfp36 level and its influence on clinical indicators in RCC patients was analyzed. After confirming transfection efficacy of sh-Zfp36 in Caki-1 and 786-O cells, changes in proliferation and apoptosis were assessed by cell counting kit-8 (CCK-8), colony formation and flow cytometry. Molecular mechanisms of Zfp36 on its downstream gene KLF10, and their involvement in the development of RCC were finally explored. Zfp36 was upregulated in RCC tissues than paracancerous ones. High level of Zfp36 predicted advanced tumor staging in RCC. Knockdown of Zfp36 attenuated proliferative ability and triggered apoptosis in Caki-1 and 786-O cells. KLF10, the downstream gene binding Zfp36, was downregulated in RCC tissues. A negative correlation was identified between expression levels of Zfp36 and KLF10. Knockdown of KLF10 abolished regulatory effects of Zfp36 on RCC phenotypes. Zfp36 is related to tumor staging in RCC patients. It regulates proliferative potential and apoptosis in RCC via negatively regulating KLF10.