Expression of the long noncoding RNA (lncRNA) metastasis-associated lung adenocarcinoma transcript 1 () correlates with tumor progression and metastasis in many tumor types. However, the impact and mechanism of action by which promotes metastatic disease remain elusive. Here, we used CRISPR activation (CRISPRa) to overexpress in patient-derived lung adenocarcinoma (LUAD) cell lines and in the autochthonous K-ras/p53 LUAD mouse model. overexpression was sufficient to promote the progression of LUAD to metastatic disease in mice. Overexpression of enhanced cell mobility and promoted the recruitment of protumorigenic macrophages to the tumor microenvironment through paracrine secretion of CCL2/Ccl2. up-regulation was the result of increased global chromatin accessibility upon overexpression. Macrophage depletion and Ccl2 blockade counteracted the effects of overexpression. These data demonstrate that a single lncRNA can drive LUAD metastasis through reprogramming of the tumor microenvironment.
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