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Long intergenic non-coding RNA-  Nucleotide Metabolism Regulator (lincNMR ) is a long non-coding RNA (lncRNA) which is induced in hepatocellular carcinoma. Its depletion invokes a proliferation defect, triggers senescence and inhibits colony formation in liver, but also breast and lung cancer cells. Triple-label SILAC proteomics profiles reveal a deregulation of key cell cycle regulators in  lincNMR -depleted cells like the key dNTP synthesizing enzymes RRM2, TYMS and TK1, implicating  lincNMR  in regulating nucleotide metabolism.  LincNMR  silencing decreases dNTP levels, while exogenous dNTPs rescues the proliferation defect induced by  lincNMR  depletion. In vivo RNA Antisense Purification (RAP-MS) identifies YBX1 as a direct interaction partner of  lincNMR  which regulates RRM2, TYMS and TK1 expression and binds to their promoter regions. In a Chick Chorioallantoic Membrane (CAM) in vivo model,  lincNMR -depleted tumors are significantly smaller. In summary, we discover a lincRNA,  lincNMR , which regulates tumor cell proliferation through a YBX1-RRM2-TYMS-TK1 axis governing nucleotide metabolism.

The lncRNA lincNMR regulates nucleotide metabolism via a YBX1 - RRM2 axis in cancer