Here, we aimed to focus on the function of zinc and its underlying mechanism in CRC and determine whether CRIP1 promotes invasion and CRC metastasis through excessive zinc-induced epithelial-mesenchymal transition (EMT) by affecting the phosphorylated glycogen synthase kinase (GSK)-3beta.
The present study provides new evidence that abnormal expression of CRIP1 might be related to the degree of metastasis in colorectal cancer and that CRIP1 silencing could effectively inhibit migration and invasion during colorectal cancer development.
In Kaplan Meier analyses, CRIP1 expression was significantly associated with the distant metastases-free survival of patients, revealing a better prognosis for high CRIP1 expression (p = 0.039).
Interestingly and contrarily to gastric cancer, we found CRIP1 expression more frequently in patients with long‑term survival (10-year survival 73% in positive vs. 54% in negative cases, p = 0.0433) and without metastases (p = 0.0108) indicating a favorable prognostic effect.