COX-2 regulates E-cadherin expression through the NF-κB/Snail signaling pathway in gastric cancer
Authors: Hailong Li
Liang Qiao
Zhaofeng Chen
Min Liu
Qian Ren
Xiaojun Liu
Yongning Zhou
Bo Song
Linlin Li
Shanshan Huang
Zenan Hu
Journal: International Journal of Molecular Medicine (2013)
Discipline: CLINICAL MEDICINE
Keywords: COX-2; E-cadherin; NF-κB; Snail; gastric cancer
Affiliations: Division of Gastroenterology and Hepatology, The First Hospital of Lanzhou University, Lanzhou, Gansu, P.R. China.

Abstract:  Cyclooxygenase-2 (COX-2) participates in cancer invasion and metastasis by decreasing the expression of E-cadherin. However, the molecular mechanisms through which COX-2 regulates E-cadherin expression and function have not yet been fully elucidated. The aim of this study was to investigate the possible molecular mechanisms through which COX-2 regulates E-cadherin expression in gastric cancer. The mRNA and protein expression of COX-2, nuclear factor-κB (NF-κB), Snail and E-cadherin was detected in gastric cancer cells by quantitative PCR and western blot analysis, respectively. The expression of these genes was also detected in healthy gastric mucosa and gastric cancer tissues by immunohistochemistry. We detected various levels of COX-2, nuclear factor-κB (NF-κB), Snail and E-cadherin expression in the normal gastric mucosa and cancer tissues; however, the expression patterns differed: the increased expression of COX-2, NF-κB and Snail was observed in the gastric cancer tissues, whereas there was a considerable reduction in E-cadherin expression in the cancer tissues compared to the normal gastric mucosa. The expression patterns of COX-2, NF-κB and Snail were similar. The increased expression of COX-2 in the gastric cancer tissues closely correlated with the increased expression of NF-κB and Snail, but inversely correlated with the expression of E-cadherin. Treatment of the SGC7901 cells (which express high levels of COX-2) with celecoxib, a COX-2 inhibitor, not only led to a marked dose- and time-dependent decrease in the expression of COX-2, NF-κB and Snail, but also led to a significant increase in the expression of E-cadherin, and this was associated with a reduction in cell invasion. By contrast, the same treatment did not alter the expression of these genes in another gastric cancer cell line, MGC803 (which barely expresses COX-2). These data suggest that COX-2 regulates the expression of E-cadherin through the NF-κB and Snail signaling pathway in gastric cancer. 

Retracted: No

PubPeer comments:
 Figure 4. Image duplication. ![file] , 
 Corrigendum, [11 January 2022] .  Following the publication of the above article, an interested reader drew to the author s attention that Fig. 4 contained a duplication error, which arose during the assembly of the figure; specifically, the upper-left panel in Fig. 4, showing the result of the u2018Control in 12 hu2019 experiment, was inadvertently repeated with the u2018Control in 48 hu2019 panel. The corrected version of Fig. 4, showing the correct data for the u2018Control in 12 hu2019 experiment, is shown below. The authors can confirm that this error does not change either the interpretation or the original conclusions of this study. The authors are grateful to the Editor of *International Journal of Molecular Medicine* for granting them the opportunity to publish the Corrigendum, and all the authors agree with this correction. Furthermore, the authors apologize to the readership for any inconvenience caused. ,