As tumourigenesis progressed, however, reduced Rbm5 expression lead to significantly more aggressive lung cancer i.e. increased adenocarcinoma nodule numbers and tumour size.
Our study demonstrated that EGFR expression is regulated by RBM5 in lung adenocarcinomas cells either in a direct or indirect way, which might be meaningful with regards to target therapy in lung cancer.
NUMB alternative splicing, which is frequently altered in lung cancer, can regulate colony and xenograft tumor formation, and its modulation recapitulates or antagonizes the effects of RBM5, 6, and 10 in cell colony formation.
On the basis of the existing data, we suggest that-to more thoroughly assess the potential involvement of RBM5 as a lung cancer regulatory protein-more research is required regarding (a) the expression of not only full-length RBM5 but all of the alternate variants associated with the locus, in relation to histologic subtype and smoking history, and (b) the mutation status of various genes within the transforming growth factor-alpha signaling pathway, which may function to either directly or indirectly regulate RBM5 activity in RBM5-retaining lung cancers.
In addition, we found that RBM5 protein expression loss in primary lung tumors is correlated with increased lymph node metastasis in a small number of lung cancer patients.