[ABSTRACT]AIM:ToinvestigatetheroleoftinyantisensenucleicacidagainstmiR-155(tinyantimiR-155, t-antimiR-155) in multiple myeloma cells .METHODS:According to the seed sequence of miR-155, t-antimiR-155 was designed and synthesized .t-antimiR-155 was transfected by Lipofectamine TM 2000 into RPMI-8266 cells.The cells were di-vided into t-antimiR-155 group, scrambled control (SCR) group and blank control group .The growth-inhibitory potencies were measured by MTT assay .The ability of cell colony formation was detected by cell colony formation assay .The cell ap-optosis was assessed by flow cytometry with annexin V /PI double staining .RESULTS: The best concentration and time were 0.4 μmol/L and 48 h, respectively.The cell colony forming experiment showed that the circumstances of forming cell community in t-antimiR-155 group was weaker than that in SCR group , and the colony formation inhibitory rate of former was significant higher than the latter .Compared with SCR group , the cell apoptosis in t-antimiR-155 group significantly in-creased.CONCLUSION: The t-antimiR-155 inhibits the progression of multiple myeloma cells by interfering with miR-155.miR-155 may serve as a potential target in gene therapy for treating multiple myeloma .

AIM:TostudythefunctionofmicroRNA(miR)-19aandmiR-92abyseed-targetinginhibitionin multiple myeloma cells and their signal pathways .METHODS:The experiments were divided into t-antimiR-19a group, t-antimiR-92a group, scramble control group and blank control group .The growth-inhibitory potencies were measured by MTT assay.The ability of cell colony formation was measured by cell colony formation assay .The ability of cell invasion was measured by Transwell experiment .The miR-19a and miR-92a target gene signal pathways were integrated by miRFo-cus software.RESULTS:MTT assay showed that t-antimiR-19a and t-antimiR-92a significantly inhibited the viability of multiple myeloma cells , and the best concentration and time were 0.5μmol/L and 48 h, respectively .The colony number in t-antimiR-19a/92a group was less than that in scramble control group .The transfection with t-antimiR-19a or t-antimiR-92a effectively decreased the cell invasion , as the relative invasion cell number was significantly decreased compared with scramble control group.miR-19a and miR-92a were involved in mTOR signaling, cell cycle and other cancer pathways . CONCLUSION:miR-19a and miR-92a cluster might be a potential target for therapeutic intervention in multiple myelo-ma.