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.

Automated summary

In this study, the high expression of chimeric RNA RRM2-C2orf48 was found to be significantly correlated with lymph node metastasis, distant metastasis, TNM stage, and smoking in lung cancer patients and cell lines. Overexpressing RRM2-C2orf48 promoted cell growth and accelerated the NNK-induced lung cancer process. The knockdown of RRM2-C2orf48 inhibited the growth of RRM2-C2orf48-overexpressing cells, and miR-219a-2-3p was identified as a potential target of RRM2-C2orf48 in lung cancer.