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Overexpression of FER1L4 promotes the apoptosis and suppresses epithelial-mesenchymal transition and stemness markers via activating PI3K/AKT signaling pathway in osteosarcoma cells

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单位: [1]Department of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, 100050, PR China [2]Department of Medicine, College of Medicine and Life Sciences, University of Toledo, Ohio, 43614, USA
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关键词: FER1L4 Apoptosis EMT Stemness PI3K/AKT Osteosarcoma

摘要:
Novel long non-coding RNA Fer-l-like protein 4 (FER1L4) has been identified as a tumor suppressor in endometrial carcinoma, ovarian cancer, hepatocellular carcinoma, esophageal squamous cell carcinoma. However, the function of FER1L4 in osteosarcoma has not been clear. The aim of the research was to explore the effects of FER1L4 in osteosarcoma. Results showed that FER1L4 was observed to be lowly expressed in osteosarcoma cell lines (US-O2, MG-63 and SaOS-2 cells), especially MG63 cells. Besides, overexpression of FER1L4 remarkably repressed the proliferation, migration and invasion of MG63 cells. FER1L4-induced apoptotic cell death leaded to the activation of caspase-3 and Bax/Bcl2. Moreover, epithelial-mesenchymal transition (EMT) was tremendously suppressed by increased FER1L4, evidences were the increased E-cadherin and reduced vimentin and fibronectin. Blocking FER1L4 expression by sh-FER1L4 treatment increased the expression of SOX9, CD44, ALDH1, Nanog and Oct4, indicating that FER1L4 could effectively decrease cell stemness in osteosarcoma. Furthermore, the protein levels of p-AKT and p-PI3K were remarkably suppressed when FER1L4 was knocked down. In conclusion, the study indicated that FER1L4 acted as a tumor suppressor in osteosarcoma via activating PI3K/AKT pathway may be a new prognostic biomarker and potential therapeutic target for osteosarcoma intervention.

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出版当年[2018]版:
大类 | 4 区 医学
小类 | 4 区 病理学
最新[2025]版:
大类 | 4 区 医学
小类 | 3 区 病理学
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出版当年[2017]版:
Q3 PATHOLOGY
最新[2023]版:
Q2 PATHOLOGY

影响因子: 最新[2023版] 最新五年平均[2021-2025] 出版当年[2017版] 出版当年五年平均[2013-2017] 出版前一年[2016版] 出版后一年[2018版]

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第一作者单位: [1]Department of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, 100050, PR China
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通讯机构: [1]Department of Orthopaedics, Beijing Friendship Hospital, Capital Medical University, 100050, PR China [*1]No. 95 Yong An Road, Xi Cheng District, Beijing, 100050, PR China.
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