Published online Jan 28, 2018. doi: 10.3748/wjg.v24.i4.475
Peer-review started: October 25, 2017
First decision: November 14, 2017
Revised: November 23, 2017
Accepted: November 28, 2017
Article in press: November 28, 2017
Published online: January 28, 2018
Processing time: 95 Days and 13.3 Hours
Colorectal cancer (CRC) is the third leading cancer and the third most frequent cause of cancer-related death in the United States. Cell cycle-related and expression-elevated protein in tumor (CREPT) is preferentially expressed in many kinds of carcinomas. However, the correlation between CREPT and CRC clinicopathological patterns remains unclear. Study of the impact of CREPT expression on the anticancer drug 5-fluorouracil (5-FU) resistance in CRC has been limited.
We investigated the expression pattern of CREPT in CRC and explored if CREPT rendered CRC cells sensitive to 5-FU.
We investigated the expression pattern of CREPT in CRC. To the best of our knowledge, this is the first study to explore the correlation between CREPT and CRC cell sensitivity to 5-FU. Our results lead us to consider CREPT as a potential chemotherapy predictive biomarker. Moreover, further study on the impact of CREPT on chemotherapy outcome in other cancers and on other antitumor drugs is needed.
We analyzed tissue sections from 203 primary CRC patients and 13 benign colorectal adenoma patients using immunohistochemistry with anti-CREPT antibody. CREPT overexpressing/knockdown cell lines were established by lentivirus infection. Expression of CREPT in these cell lines was analyzed by western blotting and the cell viability was measured by CCK-8 assay. The cell lines were subjected to 5-FU treatment. The cytotoxic effect of 5-FU was measured by CCK-8 assay and poly (ADP-ribose) polymerase/flow cytometry analysis.
CREPT expression correlates with clinicopathological features in CRC. CREPT was abundantly expressed in CRC tissues compared with benign tissues. A significant increase in CREPT was detected in more highly differentiated tumors. The intensive staining signal was enriched in the malignant region in contrast to the margin and normal counterparts in the same slide. CREPT stimulated cell proliferation and the cell cycle in CRC cells. Cell growth was significantly enhanced when CREPT was overexpressed via exogenous transfection, while CREPT depletion markedly suppressed cell viability. Overexpression of CREPT sensitized CRC cells to 5-FU-induced apoptosis. Knock down of CREPT markedly suppressed cell proliferation. However, viability of CREPT-silenced DLD1 cells was significantly increased in comparison with control cells in response to 5-FU treatment, indicating that drug resistance was induced by CREPT deficiency. 5-FU elicited dramatic apoptosis in DLD1 cells.
The impact of CREPT on CRC cell response to 5-FU was identified for the first time. We hypothesize that this phenomenon is attributed to an accelerated cell cycle induced by high expression of CREPT. However, the mechanism of this finding requires further study. Clinically, biomarkers for chemotherapy efficacy prediction are urgently needed and this research provides a candidate.
There were a few limitations to this study. For example, compared to a public database, first-hand follow-up data of patients are more convincing. For the future, we are working on animal experiments to verify our findings in vivo. Then, we will investigate the mechanisms of action of CREPT, and the possibility of clinical application of CREPT as a prognostic indicator.