The Regulation Of The Inhibitor Of BTK To MiR-21in Mesenchymal Stem Cells

Objectives Mesenchymal stem cells which have the ability of the tumor homing, notonly involved in the constituting of tumor microenvironment but also promoted tumorgrowth by tumor-cell interactions. However, mesenchymal stem cell transplantation itselfhas the potential tumorigenicity for non-cancer patients. Bruton’s Tyrosine Kinase (BTK)is a member of the tyrosine kinase subfamily. Monocytes and other myeloid cells were allBTK expression except for end-stage development plasma cells of T, B lymphocyte. Theexcessive activation of BTK may lead to the activation of downstream signaling pathwaysand cell transformation and proliferation, finally may resistant to apoptosis. However,whether mesenchymal stem cells express BTK, there were not reported currently. Thus,this experiment focuses on whether mesenchymal stem cells that drived from normal andpatient express BTK or not, and observe whether the inhibitor of BTK will inhibitor thegrowth of the mesenchymal stem cells.At the same time we research whether the oncogenedown-regulation or not in mesenchymal stem cells after the application of BTK inhibitorwhich provides a new idea for future anti-tumor from the tumor microenvironment andreduce the risk of tumorigenicity which generated by mesenchymal stem cells.Methods The umbilical cord mesenchymal stem cells was identified by flow cytometry.And the Western blotting was used to detect the expression of BTK in a variety of sourcesof mesenchymal stem cells. Then we use MTT to detect the inhibition rate of themesenchymal stem cells after the application of BTK inhibitor-Ibrutinib. Afterwards, theexpression of the cancer gene miR-21exist in mesenchymal stem cells was measured byRT-PCR.Results The BTK expressed in mesenchymal stem cells derived from umbilical cord,normal bone marrow and myeloma patients. After the application of BTK inhibitor-Ibrutinib at different concentrations to the mesenchymal stem cell,the inhibition ratio wasdifferent,and the cancer gene miR-21expressed by mesenchymal stem cells was down-regulated.Conclusions1There were stably expressing BTK in different sources of mesenchymalstem cells;2The BTK inhibitor Ibrutinib could inhibit the proliferation of mesenchymalstem cells;3The BTK inhibitor Ibrutinib could reduce the expression of the cancer genemiR-21expressed by mesenchymal stem cells.