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Expression of PER, CRY, and TIM genes for the pathological features of colorectal cancer patients

Authors Wang Y, Cheng Y, Yu G, Jia B, Hu Z, Zhang L

Received 23 September 2015

Accepted for publication 22 January 2016

Published 5 April 2016 Volume 2016:9 Pages 1997—2005

DOI https://doi.org/10.2147/OTT.S96925

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Dr Ram Prasad

Peer reviewer comments 3

Editor who approved publication: Professor Daniele Santini


This paper has been retracted 
 
Yong Wang,1 Yunsheng Cheng,1 Gang Yu,1 Benli Jia,1 Zhihang Hu,1 Lijiu Zhang2

1Department of General Surgery, 2Department of Gastroenterology, The Second Affiliated Hospital of Anhui Medical University, Hefei, People’s Republic of China

Abstract: As typical clock gene machinery, period (PER1, PER2, and PER3), cryptochrome (CRY1 and CRY2), and timeless (TIM), could control proliferation, cellular metabolism, and many key functions, such as recognition and repair of DNA damage, dysfunction of the circadian clock could result in tumorigenesis of colorectal cancer (CRC). In this study, the expression levels of PER1, PER2, and PER3, as well as CRY1, CRY2, and TIM in the tumor tissue and apparently healthy mucosa from CRC patients were examined and compared via quantitative real-time polymerase chain reaction. Compared with the healthy mucosa from CRC patients, expression levels of PER1, PER2, PER3, and CRY2 in their tumor tissue are much lower, while TIM level was much enhanced. There was no significant difference in the CRY1 expression level. High levels of TIM mRNA were much prevalent in the tumor mucosa with proximal lymph nodes. CRC patients with lower expression of PER1 and PER3 in the tumor tissue showed significantly poorer survival rates. The abnormal expression levels of PER and TIM genes in CRC tissue could be related to the genesis process of the tumor, influencing host–tumor interactions.

Keywords: colorectal cancer, cancer chronotherapy, period genes, cryptochrome genes, timeless gene

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