CGRP: A New Endogenous Cell Stemness Maintenance Molecule

Figure 4

Abnormal CGRP expression promotes cell cycle disorder and promotes the occurrence of pancreatic cancer. The helicase Prp2 (blue) and the coactivator Spp2 (purple) combine stably with the anchor molecules on the spliceosome, so as to binding Prp2 to the activated spliceosome and allowing a greater role for Prp2. CGRP pre-mRNA (red) is loaded into the characteristic channel between the N- and C-halves of Prp2. The process of ATP binding and hydrolyzation or trypsin (green, specific high expression in the pancreas) triggers Prp2 to move into sensitive binding site of trypsin, driving pre-mRNA to move unidirectionally and gradually towards its 3 end. By CGRP disturbing cell cycle, abnormal shearing breaks the genetic stability and amplifies oncogenic signals, whose function is similar to that of an essential translator and amplifier in the carcinogenic pathway.