Colorectal Cancer
Copyright ©The Author(s) 2003. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Gastroenterol. Aug 15, 2003; 9(8): 1725-1728
Published online Aug 15, 2003. doi: 10.3748/wjg.v9.i8.1725
Effect of retinoic acid on cell proliferation kinetics and retinoic acid receptor expression of colorectal mucosa
Hong-Bo Wei, Xiao-Yan Han, Wei Fan, Gui-Hua Chen, Ji-Fu Wang
Hong-Bo Wei, Xiao-Yan Han, Department of Gastrointestinal Surgery, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China
Wei Fan, Department of Nuclear Medicine, Cancer Center, Sun Yat-Sen University, Guangzhou 510060, China
Gui-Hua Chen, Ji-Fu Wang, Department of Gastrointestinal Surgery, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510080, China
Author contributions: All authors contributed equally to the work.
Supported by Natural Science Foundation of Guangdong Province, No.010742
Correspondence to: Dr. Hong-Bo Wei, Department of Gastrointestinal Surgery, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510630, China. drwhb@21cn.com
Telephone: +86-20-85516867 Ext 2228
Received: August 24, 2002
Revised: September 12, 2002
Accepted: February 11, 2003
Published online: August 15, 2003
Abstract

AIM: To investigate the effect of retinoic acid (RA) on cell proliferation kinetics and retinoic acid receptor (RAR) expression of colorectal mucosa.

METHODS: One hundred sixty healthy male Wistar rats were randomly divided into 4 groups. Rats in groups I and II were subcutaneously injected with dimethylhydrazine (DMH) (20 mg/kg, once a week,) for 7 to 13 weeks, while groups III and IV were injected with normal saline. Rats in groups II and III were also treated with RA (50 mg/kg, every day, orally) from 7th to 15th week, thus group IV was used as a control. The rats were killed in different batches. The expressions of proliferating cell nuclear antigen (PCNA), nucleolar organizer region-associated protein (AgNOR) and RAR were detected.

RESULTS: The incidence of colorectal carcinoma was different between groups I (100%) and II (15%) (P < 0.01). The PCNA indices and mean AgNOR count in group II were significantly lower than those in group I (F = 5.418 and 4.243, P < 0.01). The PCNA indices and mean AgNOR count in groups I and II were significantly higher than those in the groups III and IV (in which carcinogen was not used) (F = 5.927 and 4.348, P < 0.01). There was a tendency in group I that the longer the induction with DMH the higher PCNA index and AgNOR count expressed (F = 7.634 and 6.826, P < 0.05). However, there was no such tendency in groups II, III and IV (F = 1.662 and 1.984, P > 0.05). The levels of RAR in normal and cancerous tissues in groups treated with RA were significantly higher than those in groups not treated with RA (F = 6.343 and 6.024, P < 0.05).

CONCLUSION: RA decreases the incidence of colorectal carcinoma induced by DMH. Colorectal cancer tissue is associated with abnormal expression of PCNA, AgNOR and RAR. RA inhibits the expression of PCNA and AgNOR, and increases RAR concentration in colorectal tissues.

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