The results indicate that hyperplastic polyps had the lowest levels of MMP-1 and MMP-7, tubular polyps showed higher levels of both MMP-7 and MMP-14, and tubulovillous adenoma showed higher levels of MMP-1, MMP-7 and MMP-14.
Relative to immunosuppressed mice, wild mice exhibited more severe inflammatory infiltration and lung injury as well as a significant increase in myeloperoxidase and malondialdehyde levels and a decrease in superoxide dismutase level after MP infection.
The expression levels of CDX2 mRNA was significantly lower in the CRC group in comparison to HP/adenoma and control groups, P<0.05, and showed a further decrease with a higher degree of TNM staging.
The enzyme activities of matrilysin were detected in cancer tissue and adenoma tissue, whereas they were hardly detectable in hyperplastic polyps, mildly inflamed regions of ulcerative colitis, and normal colon tissue.
<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
Using tissue microarrays, PD-L1 expression in tumor cells (TCs) and immune cells (ICs) was manually scored in 197 cases and 27 cases of bladder and HP cancer, respectively.
Compared to normal colon (2 of 12, 16%) and sTAs (3 of 17, 18%), HPs (15 of 19, 79%) and TSAs (8 of 14, 57%) displayed significant inactivation of RUNX3 (P<0.05).
In vivo TLR2 gene transfer via intranasal inoculation of adenoviral vector was performed to reconstitute TLR2 expression in airway epithelium of TLR2(-/-) BALB/c mice, with or without ensuing Mp infection.
Trefoil Factor 1 showed the same trend of expression for sessile serrated adenomas as compared to hyperplastic polyps and was significantly higher in both polyps compared to tubular adenomas.
<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
Furthermore, any (1+/2+) COX-2 overexpression was more frequent in non-serrated adenomas (60% = 307/515) than in hyperplastic polyps (13% = 3/24, p < 0.0001) and serrated polyps (SSAs and mixed polyps) (25% = 3/12, p = 0.03).
<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
<i>In vitro</i> cell experiments revealed that the PI3K activity was enhanced and the PI3K/Akt pathway was significantly activated after HP infection in tumor cells, thus promoting the proliferation of tumor cells (p<0.05) in a time-dependent manner.
Adenoma samples could be distinguished from hyperplastic polyps by the expression levels of nine genes including ATP-binding cassette family A, member 8, insulin-like growth factor 1 and glucagon (sensitivity, 100%; specificity, 90.91%).
We found that: 1) SPLUNC1 protein decreased Mp levels and inhibited epithelial IL-8 production induced by Mp-derived lipoproteins; 2) normal human and mouse large airway epithelial cells expressed high levels of SPLUNC1; and 3) although Mp infection increased SPLUNC1, IL-13 significantly decreased SPLUNC1 expression and Mp clearance.
An obvious difference existed in the pattern of CK7/CK20 expression between the serrated lesions (hyperplastic polyps and serrated adenomas) and others.
In stem cells from human exfoliated deciduous teeth (SHED), HP significantly promoted calcium deposition as well as the expression of odontogenic marker genes, PANX3 and DSPP, and WNT related-genes including WNT5b and WNT16, whereas HP inhibited cell proliferation and enhanced primary cilia expression.
Both CUC-associated and sporadic hyperplastic polyps showed a substantial number of cases (46% and 64% of cases, respectively) with loss of p27 expression, and both types of lesions showed similar MIB-1 proliferation indices.
PDCD4 immunohistochemical expression was assessed in 300 polypoid lesions of the colon mucosa (50 hyperplastic polyps [HP], 50 serrated adenomas [SA], 50 tubular adenomas with low-grade-intraepithelial neoplasia [LG-IEN], 50 tubular adenomas with high-grade-IEN [HG-IEN]), and in 50 colon adenocarcinomas (CRC).
In vitro, M. pneumoniae (MP) infection to A549 cells induced the expression of CCL5, chemokines receptor 4 (CCR4), nuclear factor-κB (NF-κB) nuclear protein, and phosphorylation of NF-κB-p65 (p-NF-κB-p65), whereas NF-κB cytoplasmic protein was decreased.