Quick note for RSPO3 antagonism inhibits growth and tumorigenicity in colorectal tumors harboring common Wnt pathway mutations
Paper: RSPO3 antagonism inhibits growth and tumorigenicity in colorectal tumors harboring common Wnt pathway mutations doi: 10.1038/s41598-017-15704-y I would like to start with my rough drawing since it can help me recognize by heart now. The concept of this paper relies on Wnt signaling that contributes to the growth of colorectal tumors. Mutation of genes in Wnt pathway that related to CRC is beta-catenin, APC and RNF43 and these type of mutations are found 90% of CRC. My understanding, this paper points out the microenvironment supporting the tumor growth. Not only Wnt ligand but also R-spondin is the ligand that can activate the Wnt signaling pathway. Wnt binds to the Fz directly whereas R-spondin (RSPO) quantitatively control RNF43. RSPO binds to RNF43 which leads to proteasomal degradation, therefore, controlling the availability of Fz on the membrane. It was shown that RSPO3 antagonism worked effectively with RSPO gene fusion type (RSPO-PTPRK) in CRC...