Chimeric RNA RRM2-C2orf48 plays an oncogenic role in the development of NNK-induced lung cancer

Chimeric RNAs have been used as biomarkers and therapeutic targets for multiple types of cancers. However, less attention has been paid to their mechanism of action in neoplasia. Here, we reported that high-expressed chimeric RNA RRM2-C2orf48 was found in malignantly transformed BEAS-2B cells induced by 4-(methyl nitrosamine)-1-(3-pyridinyl)-1-butanone (NNK) in 74 lung cancer patients and several lung cancer cell lines. The expression level of RRM2-C2orf48 was significantly correlated with lymph node metastasis, distant metastasis, tumor-lymph node-metastasis (TNM) stage, and smoking. Overexpressing RRM2-C2orf48 promoted cell growth and accelerated the process of NNK-induced lung cancer. RRM2-C2orf48 knockdown inhibited the growth of RRM2-C2orf48-overexpressing BEAS-2B cells. Finally, we identified miR-219a-2-3p as a potential target of RRM2-C2orf48 in lung cancer. In summary, chimeric RNA RRM2-C2orf48 accelerated the process of NNK-induced lung cancer, and miR-219a-2-3p may be involved in this process. [Display omitted] •RRM2-C2orf48 had higher expression levels in lung cancer patients and cell lines•RRM2-C2orf48 expression was upregulated by NNK exposure•RRM2-C2orf48 played an oncogenic role in lung cancer•MiR-219a-2-3p may be a potential target of RRM2-C2orf48 Molecular biology; Cell biology; Cancer