Yapei Lu, Ziqi Cheng
Department of Gynecology, The First Hospital of Hangzhou Fuyang, Hangzhou, China
Summary
Purpose: This study aimed to explore the role and the molecular mechanism of CUL4B in the occurrence and development of ovarian cancer (OC).
Methods: The expressions of CUL4B in 20 pairs of OC tissue specimens and cell lines were detected by quantitative real-time polymerase chain reaction (qRT-PCR). Subsequently, the CUL4B knockdown and overexpression models were constructed in OC cell lines SKOV3 and A2780 using lentivirus, respectively. Transwell and cell scratch assays were used to analyze the effect of CUL4B on OC cell function. Furthermore, luciferase reporter gene experiment and rescue experiments were performed to explore the potential mechanism of CUL4B and downstream gene KLF11.
Results: The expressions of CUL4B in OC tissues were markedly higher than that of adjacent ones. Transwell and cell scratch experiments suggested that CUL4B overexpression markedly promoted the invasive and metastasis ability of OC cells. Bioinformatics and luciferase reporter gene experiments suggested that CUL4B could directly target KLF11. Rescue experiments indicated that KLF11 knockdown can reverse the inhibition of CUL4B silencing on OC cell migration and wound healing ability.
Conclusions: CUL4B expression is markedly elevated in OC tissues and cell lines. CUL4B may negatively regulate the expression of KLF11, thereby enhancing the proliferative and metastatic ability of OC. In summary, CUL4B plays an important part in the progression of OC and might serve as a new potential target and prognostic indicator for ovarian cancer treatment.
Keywords: CUL4B, KLF11, ovarian cancer, malignant progression.
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