z-logo
Premium
Expression of seven gastric cancer‐associated genes and its relevance for Wnt, NF‐κB and Stat3 signaling
Author(s) -
HAN JINGCHUN,
ZHANG KAILI,
CHEN XIAOYAN,
JIANG HAIFENG,
KONG QINGYOU,
SUN YUAN,
WU MOLI,
HUANG LEI,
LI HONG,
LIU JIA
Publication year - 2007
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0643.2007.00695.x
Subject(s) - cyclin d1 , survivin , wnt signaling pathway , cancer research , cd44 , stat3 , cancer , biology , signal transduction , microbiology and biotechnology , cell cycle , cell , genetics
The aim of the current study was to profile c‐Myc, standard CD44 (CD44s), CD44v6, cyclin D1, survivin, MMP‐7 and VEGF expression patterns in different gastric samples and to elucidate their relevance for Wnt, NF‐κB and/or Stat3 activation using multiple experimental approaches. The results revealed that 87.1% (27/31) of gastric cancers and 8.7% (2/23) of noncancerous lesions (chronic gastritis and intestinal metaplasia) showed Wnt activation (Wnt + ) that was closely related to the expression of the seven genes. Some Wnt − noncancerous lesions also expressed the above‐mentioned genes, higher frequencies of survivin (7/8), VEGF (7/8), cyclin D1 (6/8) and c‐Myc (5/8) but not CD44s (2/8), CD44v6 (3/8) and MMP‐7 (2/8) being detected in the NF‐κB + samples. Stat3 was activated in 37/54 gastric tissues, and in 3/4 VEGF, 4/6 c‐Myc, 4/8 survivin, 2/4 MMP‐7, 1/2 CD44v6, and 4/9 cyclin D1 + but Wnt − /NF‐κB − samples. These findings showed a close correlation in GCs between Wnt, NF‐κB and Stat3 signaling and expression of the seven genes, the importance of NF‐κB and Stat3 activation in regulating c‐Myc, survivin, cyclin D1 and VEGF in noncancerous lesions, and the potential coordinative effects of these three signalings on GC formation presumably by promoting the transcription of their common target genes.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here