J-M Wang1, X-J Li, J Wang. 1. Department of Imaging and Nuclear Medicine, Shanxi Medical University, Taiyuan, China. 332854663@qq.com.
Abstract
OBJECTIVE: Breast cancer (BC) is one of the most ordinary malignant tumors. Recent studies have revealed that long noncoding RNAs (lncRNAs) play an important role in the progression of tumorigenesis. This work aims to identify how circ_0067934 functions in the progression of BC. PATIENTS AND METHODS: Circ_0067934 expression of both 57 paired BC patients' tissue samples and cells was detected by Real Time-quantitative Polymerase Chain reaction (RT-qPCR). Moreover, the function of circ_0067934 was identified by performing proliferation assay, colony formation assay, cell cycle assay, and Ethynyl deoxyuridine (EdU) incorporation assay in vitro. Besides, the underlying mechanism was explored through Western blot assay and RT-qPCR. RESULTS: In this study, circ_0067934 expression was significantly higher in BC tissues when compared with that in adjacent non-tumor samples. Cell proliferation in BC was inhibited after knockdown of circ_0067934 in vitro. Moreover, cell cycle in BC was regulated after knockdown of circ_0067934 in vitro. Results of further experiments revealed that Mcl-1 was downregulated via the knockdown of circ_0067934 in BC. CONCLUSIONS: Our work suggests that circ_0067934 enhances BC cell proliferation and regulates BC cell cycle via upregulating Mcl-1.
OBJECTIVE:Breast cancer (BC) is one of the most ordinary malignant tumors. Recent studies have revealed that long noncoding RNAs (lncRNAs) play an important role in the progression of tumorigenesis. This work aims to identify how circ_0067934 functions in the progression of BC. PATIENTS AND METHODS: Circ_0067934 expression of both 57 paired BCpatients' tissue samples and cells was detected by Real Time-quantitative Polymerase Chain reaction (RT-qPCR). Moreover, the function of circ_0067934 was identified by performing proliferation assay, colony formation assay, cell cycle assay, and Ethynyl deoxyuridine (EdU) incorporation assay in vitro. Besides, the underlying mechanism was explored through Western blot assay and RT-qPCR. RESULTS: In this study, circ_0067934 expression was significantly higher in BC tissues when compared with that in adjacent non-tumor samples. Cell proliferation in BC was inhibited after knockdown of circ_0067934 in vitro. Moreover, cell cycle in BC was regulated after knockdown of circ_0067934 in vitro. Results of further experiments revealed that Mcl-1 was downregulated via the knockdown of circ_0067934 in BC. CONCLUSIONS: Our work suggests that circ_0067934 enhances BC cell proliferation and regulates BC cell cycle via upregulating Mcl-1.