Review of 'EGF/EGFR signaling axis is a significant regulator of the proteasome expression and activity in colon cancer cells'

I think that the present study entitled “EGF/EGFR signaling axis is as significant regulator of the proteasome expression and activity in colon cancer cells” is interesting, but has some defects and a bizarre and fanciful section in Discussion section.

The authors investigated the effects of EGF on mRNA expression levels of EGFR and proteasome subunits and activities of proteasome beta 5 subunits, and cell proliferation in K-ras mutant (DLD-1) colon cancer cells using RT-PCR and quantitative PCR, and fluorogenic substrate assay, and WST-1 assay, respectively.
EGF up-regulated the expression levels of EGFR and proteasome beta subunits including beta 1, 2, and 5, and activities of beta 5 subunits. AG1478 significantly abrogated these effects, but CP-724/714 did not. EGF did not promote cell proliferation in K-ras mutated cells. Oltipaz as a Nrf2 synthetic activator did not affect the expression levels of proteasome beta subunits. The authors concluded that EGF/EGFR signaling axis is as significant regulator of the proteasome expression and activity in colon cancer cells


Major
1. Introduction section is too long. Please describe concisely and succinctly.

2. In Discussion section and conclusion, authors speculated that EGF does not affect the proliferation of DLD-1 cells, possibly due to the enhanced proteolytic action of proteasome on EGFR.
This is a bizarre and fanciful speculation.
The K-ras mutations are considered to lead continuous activation of its downstream pathways.
Are the expression levels of EGFR in DLD-1 cells lower than those in K-ras wild cells due to proteolysis of EGFR? Please show whether expression levels of EGFR in DLD-1 cells are significantly low, compared with wild cells. In addition, please show how EGFR degradation by proteasomes induce cell survival.