Its Time to Consider the Lost Battle of Microdamaged Piezo2 to E. Coli when it Comes to Early Onset Colorectal Cancer

Recent identification of early onset mutational signatures with geographic variations is a significant finding by Diaz-Gay et al., since early onset colorectal cancer has emerged as an alarming public health challenge in the past two decades and we are in the dark in regards to the pathomechanism. Environmental risk factors, including lifestyle and diet are highly suspected. This is why identifying colibactin of Escherichia Coli as a potential pathogenic source in this study is one major step forward in the direction to cope with this very recent public health obstacle of our lives. Therefore, the following opinion manuscript is aiming to depict the likely onset of pathomechanism and the critical role of acquired Piezo2 channelopathy in early onset colorectal cancer that skews proton availability and proton motive force regulation on the side of E. Coli within the microbiota-host symbiotic relationship. Mechanotransduction is miraculous when it comes to converting external physical cues to inner chemical and biological ones. Correspondingly, the proposed quantum mechanical free-energy stimulated ultrafast proton-coupled tunneling, initiated by Piezo2, seems to be the principal and essential underlying novel signaling that could be lost in colorectal cancer onset, hence not only contributes to cancer initiation, lost circadian rhythms, but later to proliferation and metastasis as well.