The mechanism study of miR‐125b in occurrence and progression of multiple myeloma

Although many efforts have contributed to improve our knowledge of molecular pathogenesis about multiple myeloma ( MM ), the role and significance of micro RNA s and long noncoding RNA s in MM cells, along with the core mechanism remains virtually absent. The mRNA levels of miR‐125b and MALAT 1 in MM cell lines were detected by qRT ‐ PCR . The influence of Lenti‐Sh‐miR‐125b on cell viability and the Notch‐1 pathway‐related proteins were assessed by MTT method and western blot, respectively. We also investigated the regulation effect between MALAT 1 and Notch1 pathway. Moreover, the connection between Notch1 signaling and MM cell growth was discussed in‐depth. The reverse effect of pc DNA ‐Notch1 on the cell viability and Notch‐1 pathway proteins induced by Si‐ MALAT 1 was also studied. Furthermore, miR‐125b overexpressing MM cell lines were injected subcutaneously into nude mice. MiR‐125b and MALAT 1 were inversely expressed in MM cell lines. Lenti‐Sh‐miR‐125b inhibited the expression of MALAT 1 and Notch‐1 protein. Binding sites were confirmed between miR‐125b and MALAT 1, and silencing MALAT 1 did not alter the expression of Notch‐1. The apoptosis rate was increased and the survival rate was decreased obviously in GSI XII (targeted cleavage of Notch‐1 receptor) group, along with the inhibited Notch1 and HES 1 proteins. Moreover, the decreased cell viability and Notch‐1 pathway proteins induced by Si‐ MALAT 1 could be reversed by pc DNA ‐Notch1. Lenti‐Sh‐miR‐125b promoted survival and decreased Notch1 and HES 1 proteins levels, while this effect was reversed by si ‐ MALAT 1. MiR‐125b regulated MALAT 1 expression via Notch1 signaling pathway to regulate cell growth, thus participating in the occurrence and progression of MM , which functioned as a therapeutic target for tracking MM.