title: Possible regulatory role of Snail in NF-κB-mediated changes in E-cadherin             in gastric cancer.
abstract: In the present study, we aimed to investigate the involvement of Snail in             NF-κB-mediated changes of E-cadherin in gastric cancer. A total of 189 human gastric             cancer tissues, and 32 normal gastric mucosal tissues were used to determine the             expression levels of NF-κB, E-cadherin and Snail by immunohistochemistry. The             correlation between the expression levels and patient clinicopathological data             was analyzed. Human gastric cancer cell line SGC7901 was treated with the NF-κB             inhibitor PDTC, and the expression levels of E-cadherin and Snail were investigated             by qPCR and western blot. NF-κB, E-cadherin and Snail were all detected in normal             gastric mucosa and cancer tissues of various differentiation statuses. However,             the expression patterns of each protein were different. Strong expression of E-cadherin             was detected in normal gastric mucosa, whereas its expression gradually declined             in gastric cancer tissues, with weak expression observed in poorly differentiated             gastric cancer tissues. In contrast, weak NF-κB and Snail expressions were present             in normal gastric mucosa, while their expression levels gradually increased in             gastric cancer tissues, with the strongest expression detected in poorly differentiated             gastric cancers. The expression of E-cadherin was inversely correlated with that             of Snail and NF-κB in the tissues tested. Blockade of NF-κB using its inhibitor             PDTC led to a time-dependent reduction in Snail but a time-dependent increase             in E-cadherin in SGC7901 cells. These results suggest that in human gastric cancer,             loss of E-cadherin may be mediated through NF-κB-induced Snail upregulation. Further             studies may reveal whether targeting the NF-κB-Snail-E-cadherin axis could be             a useful approach for combating gastric cancer.
authors.affiliation: First Clinical Medical School of Lanzhou University, Lanzhou 730000, PR China.
authors.forename: Zenan
authors.initials: Z
authors.lastname: Hu
authors.forename: Xiaojun
authors.initials: X
authors.lastname: Liu
authors.forename: Zhifeng
authors.initials: Z
authors.lastname: Tang
authors.forename: Yongning
authors.initials: Y
authors.lastname: Zhou
authors.forename: Liang
authors.initials: L
authors.lastname: Qiao
mesh_terms: D000230:Adenocarcinoma / Q000378:metabolism* / Q000556:secondary; D015703:Antigens, CD; D015820:Cadherins / Q000235:genetics / Q000378:metabolism*; D045744:Cell Line, Tumor; D005260:Female; D015870:Gene Expression; D006801:Humans; D008207:Lymphatic Metastasis; D008297:Male; D008875:Middle Aged; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D011759:Pyrrolidines / Q000494:pharmacology; D000071250:Snail Family Transcription Factors; D013274:Stomach Neoplasms / Q000378:metabolism* / Q000473:pathology; D013859:Thiocarbamates / Q000494:pharmacology; D046888:Tissue Array Analysis; D014157:Transcription Factors / Q000502:physiology*
chemical_list: D015703:Antigens, CD; C513384:CDH1 protein, human; D015820:Cadherins; D016328:NF-kappa B; D011759:Pyrrolidines; D000071250:Snail Family Transcription Factors; D013859:Thiocarbamates; D014157:Transcription Factors; C020972:pyrrolidine dithiocarbamic acid