Multivariable logistic regression of cancer status in an over-dominant TGFB1rs1800469/TGFBR1 rs11568785 model demonstrated a 3.03-fold reduction in cervical cancer odds.
TGFB1T10C and XRCC1 G399A SNPs were associated with CC risk in univariate and multivariate analysis and displayed allele-dosage effects and coselection in cancer patients.
Individuals with at least one copy of the following risk alleles: T of SNP (-590C > T IL-4), C of SNP (-573G > C IL-6), A of SNP (-592C > A IL-10), T of SNP (-819C > T IL-10) and T of SNP (-509C > T TGFB1), had an adjusted odds ratio (OR) of 2.08 (95 % CI 1.475-2.934, p = 0.0001), an OR of 1.70 (95 % CI 1.208-2.404, p = 0.002), an OR of 1.87 (95 % CI 1.332-2.630, p = 0.0001), an OR of 1.67 (95 % CI 1.192-2.353, p = 0.003) and an OR of 1.91 (95 % CI 1.354-2.701, p = 0.0001), respectively, for CC.
Western blotting was performed to detect E-cadherin, vimentin, signal transducer and activator of transcription 3 (STAT3), snail family transcriptional repressor 2 (SNAIL2), phosphorylation of p70s6k (p-p70s6k) and -Pyruvate kinase M2 (PKM2) Results: TGF-β1 promoted proliferation and migration, and it attenuated apoptosis compared with cells treated with metformin with or without TGF-β1 in cervical carcinoma cells.
It has been found that certain cytokines (IL-4, IL-10 and TGF-β1) are highly expressed locally in biopsies from patients with premalignant lesions and cervical cancer, and may induce a local immune-suppression state.
VEGF and TGF-beta1 mRNA overexpression was found to be associated with progression from low-grade to high-grade cervical intraepithelial neoplasia (CIN), while YY1 showed constitutively elevated transcript levels in CIN and cervical cancer compared to controls.
Elevated expression of the oncogene c-fms and its ligand, the macrophage colony-stimulating factor-1, in cervical cancer and the role of transforming growth factor-beta1 in inducing c-fms expression.
In this study, the relationship between HPV-16 infection and the functions of three critical factors of the TGF-beta1/Smads pathway was explored to assess the possible role of E7 in the development of cervical cancer.
Vascular endothelial growth factor (VEGF), basic fibroblastic growth factor (FGF2), transforming growth factor-beta1, 2, 3 (TGFB1, 2, 3), and transforming growth factor-beta receptors (TGFBR1, 2, 3) mRNA expression pattern was evaluated in tissue samples with cervical intraepithelial neoplasia (CIN) and cervical cancer, compared to that of normal cervical tissues, and correlated to the clinical stage of the disease.
The aim of our study was to investigate the role of tumor cell-derived TGF-beta(1) on the amount of intratumoral stroma; the deposition of collagen IV, fibronectin, and laminin; and the tumor infiltrate in cervical carcinoma.
It has been suggested that squamous cell carcinomas are devoid of TGF-beta1, raising the possibility that elevated levels of this growth factor could protect against cervical cancer.
It has been proposed that loss of sensitivity to growth inhibition by TGF-beta 1 may be an important step in the development of cervical carcinoma, but it remains unclear whether this represents an early or a late event.