Effects of FOSL1 silencing on osteosarcoma cell proliferation, invasion and migration through the ERK/AP-1 signaling pathway

文献类型： 外文期刊

第一作者： Han, Yu

作者： Han, Yu;Zhao, Xingyu;Liu, Jianguo;Sun, Yifu;Sui, Yutong

作者机构：

关键词： apoptosis; extracellular-signal-regulated kinase (ERK); activator protein-1 (AP-1) signaling pathway; Fos-like antigen-1 (FOSL1); gene silencing; invasion; migration; osteosarcoma (OS); proliferation

期刊名称：JOURNAL OF CELLULAR PHYSIOLOGY （ 影响因子：6.384； 五年影响因子：5.987 ）

ISSN： 0021-9541

年卷期： 2019 年 234 卷 4 期

页码：

收录情况： SCI

摘要： Osteosarcoma (OS), as the most frequent primary malignancy of bone, is characterized by the presence of malignant mesenchymal cells. In the current study, our aim was to explore the possible effects Fos-like antigen-1 (FOSL1) had on the silencing regarding OS cell proliferation, invasion, and migration through the activation of the extracellular-signal-regulated kinase (ERK)/activator protein-1 (AP-1) signaling pathway. After the collection of OS on top of already having the adjacent normal tissue samples, the protein positive expression rate of FOSL1 was then measured by implementing the use of immunohistochemistry and discovered that FOSL1 was robustly expressed in OS. Later, to better grasp the impact FOSL1 projects on OS and its underlying mechanism, we determined the OS related genes as well as the ERK/AP-1 signaling pathway related genes expression by using a reverse-transcription quantitative polymerase chain reaction and western blot assay techniques. The results of the aforementioned two experiments revealed that the FOSL1 depletion had downregulated the expression of OS related genes by simultaneously downregulating the ERK/AP-1 signaling pathway. Moreover, cell proliferation, cycle, apoptosis, invasion, and migration of FOS1 were all tested by using a cell counting kit-8 assay, flow cytometry, Transwell assay, and scratch test, and these results presented that silencing of the FOSL1 gene inhibited OS cell proliferation, invasion, and migration. Our findings revealed a novel mechanism by which FOSL1 depletion played a significantly negative role in the OS progression through the regulation of theERK/AP-1 signaling pathway. Functional suppression of FOSL1 might be a future therapeutic strategy regarding OS.

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