Conversely, increased TGF-β1 and activated TGF-βRI and Smad3 have all been shown to have tumor-promoting effects in experimental systems of human and mouse SCCs.
Immunohistochemical Study of TGF-β1 in Oral Leukoplakia and Oral Squamous Cell Carcinoma: Correlations Between Clinicopathologic Factors and Overall Survival.
Nintedanib dose-dependently inhibited the TGF-β1-induced expression of a panel of pro-fibrotic activation markers in both ADC-TAFs and control fibroblasts derived from uninvolved lung parenchyma, whereas such inhibition was very modest in SCC-TAFs.
Immunohistochemical Expression of CD105 and TGF-β1 in Oral Squamous Cell Carcinoma and Adjacent Apparently Normal Oral Mucosa and its Correlation With Clinicopathologic Features.
We incubated the p16-positive CERV196 and p16-negative HNSCC22B SCC cell lines with EGF and EGF/TGFβ1 (10 ng/ml) and detected E-cadherin, vimentin and β-catenin by immunocytochemistry and enzyme-linked immunosorbent assay after 5, 24 and 96 h.
The transforming growth factor beta-1 (TGFβ-1-509 C/T) polymorphism was inversely associated with having an oral SCCA among persons homozygous for the recessive variant (ORcrude = 0.27; 95% CI 0.09-0.79).
TGF-β1 protein and its receptor I (TGF-βR1) were overexpressed in urine samples in malignant group compared with chronic cystitis and in SQCC group compared with TCC group.
Inhibition of TGF-beta1 suppresses motility and invasiveness of oral squamous cell carcinoma cell lines via modulation of integrins and down-regulation of matrix-metalloproteinases.
The expression levels of TGF-beta1 and its type I and type II receptors (TbetaRI and TbetaRII) were assessed by immunohistochemical and Western blot analyses in 22 oral squamous cell carcinoma lesions, in their normal adjacent mucosa and in the squamous carcinoma cell lines FaDu and CAL27.
Because transforming growth factor beta1 (TGF-beta1) is up-regulated in OSCC tumors, we examined the relationship between TGF-beta1 signaling and MMP-9 in human OSCC specimens.
A study in this issue of Cancer Cell shows that mice with a targeted knockout of the type II TGFbeta receptor in stratified epithelia specifically develop spontaneous squamous cell carcinomas in the anogenital region, but not in the skin.
Increased expression of c-Ski as a co-repressor in transforming growth factor-beta signaling correlates with progression of esophageal squamous cell carcinoma.