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The microRNA-212/132 cluster regulates B cell development by targeting Sox4.


ABSTRACT: MicroRNAs have emerged as key regulators of B cell fate decisions and immune function. Deregulation of several microRNAs in B cells leads to the development of autoimmune disease and cancer in mice. We demonstrate that the microRNA-212/132 cluster (miR-212/132) is induced in B cells in response to B cell receptor signaling. Enforced expression of miR-132 results in a block in early B cell development at the prepro-B cell to pro-B cell transition and induces apoptosis in primary bone marrow B cells. Importantly, loss of miR-212/132 results in accelerated B cell recovery after antibody-mediated B cell depletion. We find that Sox4 is a target of miR-132 in B cells. Co-expression of SOX4 with miR-132 rescues the defect in B cell development from overexpression of miR-132 alone, thus suggesting that miR-132 may regulate B lymphopoiesis through Sox4. In addition, we show that the expression of miR-132 can inhibit cancer development in cells that are prone to B cell cancers, such as B cells expressing the c-Myc oncogene. We have thus uncovered miR-132 as a novel contributor to B cell development.

SUBMITTER: Mehta A 

PROVIDER: S-EPMC4577845 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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The microRNA-212/132 cluster regulates B cell development by targeting Sox4.

Mehta Arnav A   Mann Mati M   Zhao Jimmy L JL   Marinov Georgi K GK   Majumdar Devdoot D   Garcia-Flores Yvette Y   Du Xiaomi X   Erikci Erdem E   Chowdhury Kamal K   Baltimore David D  

The Journal of experimental medicine 20150914 10


MicroRNAs have emerged as key regulators of B cell fate decisions and immune function. Deregulation of several microRNAs in B cells leads to the development of autoimmune disease and cancer in mice. We demonstrate that the microRNA-212/132 cluster (miR-212/132) is induced in B cells in response to B cell receptor signaling. Enforced expression of miR-132 results in a block in early B cell development at the prepro-B cell to pro-B cell transition and induces apoptosis in primary bone marrow B cel  ...[more]

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