Contributions
Abstract: PB1940
Type: Publication Only
Background
Long non-coding RNA maternally expressed gene 3 (MEG3) plays a critical role in cancer progression and metastasis. However, the overall biological role and regulatory mechanism of MEG3 in multiple myeloma (MM) development and progression remains largely unknown.
Aims
To explore the tumor suppression role of lncRNA MEG3 in MM and further reveal the mechanism of MEG3 functions as ceRNA to contribute to MM pathogenesis.
Methods
MEG3 expression was measured in MM patients by real-time PCR. The effect of MEG3 on cell apoptosis, cell proliferation and angiogenesis were gained from CCK-8, flow cytometric analysis and transwell invasion assays in MM cell lines ARP-1 and LP-1. Insights of the mechanism of competitive endogenous RNA (ceRNA) were gained from bioinformatic analysis, luciferase reporter assays and RNA binding protein immunoprecipitation (RIP) assay.
Results
MEG3 expression was significantly decreased in MM patients with advanced stage disease (ISS II and III) and poor prognosis.Overexpression of MEG3 promoted cell apoptosis and inhibited cell proliferation, migration and angiogenesis in MM ARP1 and LP-1 cell lines. Furthermore, MEG3 increase the expression of phosphatase and tensin homolog (PTEN) and consequentially inhibit MM cell proliferation and angiogenesis through sponging miR-181a in vitro. miR-181a mimics can limit the promotion of PTEN by MEG3.
Conclusion
MEG3 functions as a tumor suppressor in MM. High expression of MEG3 is a marker for good survival. We reveal a novel mechanism that MEG3 as a ceRNA of the PTEN gene by competing for miRNA-181a binding sites and thereby regulate the expression of the PTEN mRNA.
Session topic: 13. Myeloma and other monoclonal gammopathies - Biology
Keyword(s): Multiple Myeloma
Abstract: PB1940
Type: Publication Only
Background
Long non-coding RNA maternally expressed gene 3 (MEG3) plays a critical role in cancer progression and metastasis. However, the overall biological role and regulatory mechanism of MEG3 in multiple myeloma (MM) development and progression remains largely unknown.
Aims
To explore the tumor suppression role of lncRNA MEG3 in MM and further reveal the mechanism of MEG3 functions as ceRNA to contribute to MM pathogenesis.
Methods
MEG3 expression was measured in MM patients by real-time PCR. The effect of MEG3 on cell apoptosis, cell proliferation and angiogenesis were gained from CCK-8, flow cytometric analysis and transwell invasion assays in MM cell lines ARP-1 and LP-1. Insights of the mechanism of competitive endogenous RNA (ceRNA) were gained from bioinformatic analysis, luciferase reporter assays and RNA binding protein immunoprecipitation (RIP) assay.
Results
MEG3 expression was significantly decreased in MM patients with advanced stage disease (ISS II and III) and poor prognosis.Overexpression of MEG3 promoted cell apoptosis and inhibited cell proliferation, migration and angiogenesis in MM ARP1 and LP-1 cell lines. Furthermore, MEG3 increase the expression of phosphatase and tensin homolog (PTEN) and consequentially inhibit MM cell proliferation and angiogenesis through sponging miR-181a in vitro. miR-181a mimics can limit the promotion of PTEN by MEG3.
Conclusion
MEG3 functions as a tumor suppressor in MM. High expression of MEG3 is a marker for good survival. We reveal a novel mechanism that MEG3 as a ceRNA of the PTEN gene by competing for miRNA-181a binding sites and thereby regulate the expression of the PTEN mRNA.
Session topic: 13. Myeloma and other monoclonal gammopathies - Biology
Keyword(s): Multiple Myeloma