TGF-beta 1 and EGF regulation of PTH-rP gene expression in squamous cell carcinomas of gynecologic origin is unique for each cell line studied and different from that in human lung carcinoid cells.
A significant majority of a new series of human SCC cell lines were found to be as sensitive as primary human epidermal keratinocytes to TGF-beta 1 growth inhibition.
A panel of 45 formalin-fixed and paraffin-embedded NSCLC specimens showed positive immunostaining for TGF-beta 1, TGF-beta RI, and TGF-beta RII, with reduced TGF-beta RII in poorly differentiated adenocarcinomas and squamous cell carcinomas and some moderately differentiated adenocarcinomas.
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.
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.
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.
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).
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.
Immunohistochemical Expression of CD105 and TGF-β1 in Oral Squamous Cell Carcinoma and Adjacent Apparently Normal Oral Mucosa and its Correlation With Clinicopathologic Features.
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.
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.