Y Zhang1, J-L Liu, J Wang. 1. Department of Galactophore, ChuiYangLiu Hospital Affiliated to TsingHua University, Beijing, China. drzhangying@163.com.
Abstract
OBJECTIVE: The aim of this study was to explore whether SAPCD2 can affect the proliferation of breast cancer cells through YAP/TAZ, thus promoting the development of breast cancer (BCa). PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine SAPCD2 expression level in BCa tissues collected from patients in different tumor TNM-stage. The correlation between SAPCD2 expression and clinicopathological features of patients were analyzed, and the Kaplan-Meier test was used for survival analysis. In addition, after knocking down SAPCD2 in cells, qRT-PCR and Western blot were applied to analyze the expression of the related genes and proteins, respectively. Moreover, Cell Counting Kit-8 (CCK-8) and transwell experiments were conducted to detect cell viability, migration, and invasion abilities. Furthermore, the changes in cell viability and migration and invasion abilities were examined after the simultaneous overexpression of YAP. RESULTS: It was found that SAPCD2 expression levels in BCa tissues were remarkably higher than those in the normal control samples; meanwhile, patients with tumor size >3 cm or in the T3+T4 stage had a relatively higher expression of SAPCD2 than those with tumor size <3 cm or in T1+T2 stage. At the same time, the overall survival rate of BCa patients with highly expressed SAPCD2 was remarkably lower than that of patients in the low expression group. Moreover, it was found that the SAPCD2 level was correlated to the tumor size, TNM stage, and lymph node metastasis. After knocking down SAPCD2 in cells, cell viability, migration, and invasion abilities, as well as the YAP/TAZ protein expression levels were all found to be remarkably attenuated, which, however, were reversed after simultaneous overexpression of YAP in cells. CONCLUSIONS: SAPCD2 may be able to enhance the proliferation ability of BCa cells via modulating the expression of YAP/TAZ, thereby prompting the progression of BCa.
OBJECTIVE: The aim of this study was to explore whether SAPCD2 can affect the proliferation of breast cancer cells through YAP/TAZ, thus promoting the development of breast cancer (BCa). PATIENTS AND METHODS: Quantitative Real Time-Polymerase Chain Reaction (qRT-PCR) was performed to examine SAPCD2 expression level in BCa tissues collected from patients in different tumorTNM-stage. The correlation between SAPCD2 expression and clinicopathological features of patients were analyzed, and the Kaplan-Meier test was used for survival analysis. In addition, after knocking down SAPCD2 in cells, qRT-PCR and Western blot were applied to analyze the expression of the related genes and proteins, respectively. Moreover, Cell Counting Kit-8 (CCK-8) and transwell experiments were conducted to detect cell viability, migration, and invasion abilities. Furthermore, the changes in cell viability and migration and invasion abilities were examined after the simultaneous overexpression of YAP. RESULTS: It was found that SAPCD2 expression levels in BCa tissues were remarkably higher than those in the normal control samples; meanwhile, patients with tumor size >3 cm or in the T3+T4 stage had a relatively higher expression of SAPCD2 than those with tumor size <3 cm or in T1+T2 stage. At the same time, the overall survival rate of BCa patients with highly expressed SAPCD2 was remarkably lower than that of patients in the low expression group. Moreover, it was found that the SAPCD2 level was correlated to the tumor size, TNM stage, and lymph node metastasis. After knocking down SAPCD2 in cells, cell viability, migration, and invasion abilities, as well as the YAP/TAZ protein expression levels were all found to be remarkably attenuated, which, however, were reversed after simultaneous overexpression of YAP in cells. CONCLUSIONS:SAPCD2 may be able to enhance the proliferation ability of BCa cells via modulating the expression of YAP/TAZ, thereby prompting the progression of BCa.