DUAL REPLACEMENT OF LNC-MEG3 AND MIR-155 TRIGGER TUMOR SUPPRESSIVE ACTIVITY IN MULTIPLE MYELOMA

dc.AffiliationOctober University for modern sciences and Arts (MSA)
dc.contributor.authorEl-Khazragy, Nashwa
dc.contributor.authorSafwat, Gehan
dc.contributor.authorEmad, Passant
dc.date.accessioned2021-04-05T12:27:55Z
dc.date.available2021-04-05T12:27:55Z
dc.date.issued08/01/2020
dc.description.abstractan urgent need. Recent evidence demonstrated a definitive tumor suppressor role of Long non-coding RNA maternally expressed gene 3 (MEG3) and miR-155 in Multiple Myeloma (MM), however, their biological role remains unclear. It has been demonstrated that both markers are downregulated in MM patients compared to healthy. Objectives: We aimed to investigate the biological effect of double hit replacement for both lnc-MEG3 and miR-155 in MM cells, and compare it with the effect of each biomarker separately. Methods: MM cells were transfected by MEG3 overexpression plasmid and miR-155 mimic, the miR-155 and lnc-MEG3 expression levels were measured by qRT-PCR. MTT assay was performed to assess the cell proliferation, cell cycle, and apoptosis were monitored by Flow cytometry analysis. Results: lnc-MEG3 and miR-155 were downregulated in MM cells. In- vitro overexpression of lnc-MEG3 and miR-155 suppresses cell proliferation, induce cell cycle arrest, and promote apoptosis, the effect was more prominent with upregulation of both markers than with each individual biomarker. Conclusion: the present data demonstrate that dual overexpression of lnc-MEG3 and miR-155 elicits a powerful dual tumor suppressor effect in MM cells, in spite they have different signaling pathways, thus providing a promising therapeutic strategy in MM patients.en_US
dc.identifier.urihttps://qrgo.page.link/vA7Li
dc.language.isoen_USen_US
dc.publisherElsevieren_US
dc.relation.ispartofseriesExperimental Hematology;Volume 88, Pages S59-S59
dc.titleDUAL REPLACEMENT OF LNC-MEG3 AND MIR-155 TRIGGER TUMOR SUPPRESSIVE ACTIVITY IN MULTIPLE MYELOMAen_US
dc.typeArticleen_US

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