Interleukin‐1β/nuclear factor‐κB signaling promotes osteosarcoma cell growth through the microRNA‐181b/phosphatase and tensin homolog axis. Issue 2 (14th September 2018)

• Record Type: Journal Article
• Authors: Wang, Weiguo; Wang, Zhengguang; Chen, Shijie; Zang, Xiaofang; Miao, Jinglei
• Is Part Of: Journal of cellular biochemistry. Volume 120:Issue 2(2019)
• Page Start: 1763
• Page End: 1772
• Publication Date: 2018-09-14
• Subjects: interleukin‐1β -- miR‐181b -- nuclear factor‐κB -- osteosarcoma -- phosphatase and tensin homolog; Cytochemistry -- Periodicals; 572
• DOI: 10.1002/jcb.27477
• Languages: English
• ISSNs: 0730-2312

Abstract

Abstract: So far, microRNA has attracted plenty of interest due to its role in tumorigenesis. Reportedly, miR‐181b may be involved in the tumorigenesis of osteosarcoma (OS). In the current study, we attempted to investigate the detailed function and mechanism of miR‐181b in OS carcinogenesis. Herein, miR‐181a, miR‐181b, miR‐181c, and miR‐181d expressions in OS tissues were higher than that in nontumor tissue samples as examined real‐time polymerase chain reaction. Via direct targeting, miR‐181b negatively regulated the expression of phosphatase and tensin homolog (PTEN), a well‐known tumor suppressor. Furthermore, a small interfering RNA strategy was used to find that interleukin (IL)‐1B and nuclear factor‐κB (NF‐κB) regulate miR‐181b and PTEN expression. Consequently, the repression of PTEN by miR‐181b promotes OS cell proliferation. In summary, our data support a critical role for NF‐κB‐dependent upregulation of miR‐181b, which further inhibited PTEN expression and promoted the cell proliferation of OS cell lines. The above findings represent a new pathway for the repression of PTEN and the promotion of cell proliferation upon IL‐1β induction. Abstract : So far, microRNA has attracted plenty of interest due to its role in tumorigenesis. Reportedly, miR‐181b may be involved in the tumorigenesis of osteosarcoma (OS). In the current study, we attempted to investigate the detailed function and mechanism of miR‐181b in OS carcinogenesis. Herein, miR‐181a, miR‐181b, miR‐181c, and miR‐181d expression in OS tissues was higher than that in nontumor tissue samples as examined real‐time polymerase chain reaction. Via direct targeting, miR‐181b negatively regulated the expression of phosphatase and tensin homolog (PTEN), a well‐known tumor suppressor. Furthermore, a small interfering RNA strategy was used to find that interleukin (IL)‐1B and nuclear factor‐κB (NF‐κB) regulate miR‐181b and PTEN expression. Consequently, repression of PTEN by miR‐181b promotes OS cell proliferation. Taken together, our data support a critical role for NF‐κB‐dependent upregulation of miR‐181b, which further inhibited PTEN expression and promoted the cell proliferation of OS cell lines. The above findings represent a new pathway for the repression of PTEN and the promotion of cell proliferation upon IL‐1β induction.