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RNA-Seq analysis of human M238P melanoma cells transduced with a lentivirus expressing the miR-143/145 cluster or a control lentivirus

ABSTRACT: RNA-Seq analysis of human M238P melanoma cells transduced with a lentivirus expressing the miR-143/145 cluster or a control lentivirus

PROVIDER: PRJNA721323 | ENA |

REPOSITORIES: ENA

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RNA-Seq analysis of human M238P melanoma cells transduced with a lentivirus expressing the miR-143/145 cluster or a control lentivirus

Project description:To assess the transcriptomic response associated with upregulation of the miR-143/-145 cluster, BRAFV600E mutant human melanoma cells M238P cells were transduced for stable expression of miR-143/145 cluster or with a control vector. Forty-eight hours after transduction, cells were treated with 1 μg/mL of puromycin for one week. RNA samples were then harvested. Two independent experiments were carried out.

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The mir-143-145 cluster plays a pro-tumorigenic role in lung adenocarcinoma by promoting neoangiogenesis

Project description:A growing body of literature has proposed cell-autonomous tumor suppressor functions for the mir-143~145 cluster in a variety of human cancers, including lung adenocarcinoma, and has reported therapeutic benefits of delivering mir-143 and mir- 145 to tumors. In contrast to these studies, we found that depletion or forced expression of mir-143 and mir-145 in an autochthonous mouse model of lung adenocarcinoma did not affect tumor development. Surprisingly, we observed that loss of mir-143~145 from the tumor microenvironment significantly reduced tumor burden, indicating a non-cell- autonomous role for these miRNAs in promoting tumorigenesis. By examining the expression patterns of different cell populations isolated in vivo from tumor-bearing lungs using an integrated computational approach, we identified a role for mir-145 in stimulating the proliferation of endothelial cells by downregulating an inhibitory kinase, Camk1d, which prevents mitotic entry. As a consequence, tumors in mir-143~145- deficient animals exhibited diminished hallmarks of neo-angiogenesis, increased apoptosis and their expansion appeared limited by the tumor’s ability to co-opt the alveolar vasculature. These findings show that expression of the mir-143~145 cluster in the tumor stroma promotes rather than suppresses tumorigenesis and cautions against the use of these miRNAs as agents in cancer therapeutics.

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Blockade of the pro-fibrotic reaction mediated by the miR-143/-145 cluster enhances the responses to targeted therapy in melanoma

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Mouse ureter: wild type vs miR-143/145 knock out

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Mouse ureter: wild type vs miR-143/145 knock out

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Analysis of miR-143/145 wild-type and null mouse intestinal myofibroblasts before and after LPS stimulation

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Breast tumor from Pik3caH1047R/+ mammary gland transduced with single or pooled lentivirus.

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