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. 2015 Sep 21;212(10):1679–1692. doi: 10.1084/jem.20150489

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© 2015 Mehta et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/3.0/).

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Figure 9. — Enforced expression of miR-132 inhibits the development of spontaneous B cell cancers in cells with the Eμ-myc transgene. (A) Cells from a pre–B cell lymphoblastic leukemia line, 70Z/3, were transduced with a control vector (MGP) or a miR-132–overexpressing vector (miR-132) and cultured for 48 h with or without LPS (20 µg/ml). The frequency of cells expressing AnnV was then measured by FACS. (B–E) C57BL/6 mice were reconstituted with donor HSPCs from WT or Eμ-myc mice that were either transduced with a control vector (MG) or miR-132 overexpressing vector (miR-132). These mice were followed for 4 mo and harvested for analysis at this time point (n = 8–10 mice per group). (B) Survival curve for all experimental cohorts (P = 0.0037). Frequency of (C) bone marrow B cells (CD19⁺), (D) myeloid cells (CD11b⁺), and (E) pre–B cells (B220⁺IgM-CD43-) in all cohorts. Data represents two independent experiments and is represented as mean ± SEM. **, P < 0.01; ***, P < 0.001, Student’s t test.