Rbm7, a component of the nuclear exosome targeting (NEXT) complex, plays diverse roles in cells. It is involved in RNA surveillance, as the NEXT complex it belongs to directs the RNA exosome for degradation of nuclear noncoding RNAs [6,7,8]. Rbm7 also activates the positive transcription elongation factor b (P-TEFb) following genotoxic stress, promoting cell viability by stimulating RNA polymerase II transcription [4,5].

In breast cancer, Rbm7 deficiency promotes metastasis. Rbm7-depleted breast cancer cells have increased lung metastasis potential, and Rbm7 controls the splicing switch of MFGE8, with MFGE8-L having an inhibitory effect on cell migration and invasion while MFGE8-S has the opposite effect. Additionally, Rbm7 negatively regulates the NF-κB cascade [1].

In lung fibrosis, increased Rbm7 expression in lung epithelial cells promotes the degradation of the long non-coding RNA NEAT1, impairs DNA repair, triggers apoptosis, and ultimately drives tissue fibrosis [2,3].

In conclusion, Rbm7 is crucial for RNA-related processes and plays significant roles in diseases such as breast cancer and lung fibrosis. Studies using gene-knockout or conditional-knockout models in these contexts have revealed its role in metastasis and fibrosis development, providing insights into potential molecular-targeted therapies.