Bioinformatic analysis was used to determine the effect of CLTC and TGFB1 expression on prognosis and overall survival in patients with hepatocellular carcinoma (HCC).
TGF-β1-induced phosphorylation of Smad2 and Akt was enhanced in RIG-I-deficient HCC spheres, knockdown of AKT gene expression abolishing the augmentation of TGF-β1-induced Smad2 phosphorylation.
Immobilized Transforming Growth Factor-Beta 1 in a Stiffness-Tunable Artificial Extracellular Matrix Enhances Mechanotransduction in the Epithelial Mesenchymal Transition of Hepatocellular Carcinoma.
The plasma expression levels of snaR and TGF-β1 were positively correlated in patients with HCC; however, not in healthy controls. snaR overexpression significantly promoted cancer cell migration and invasion, and additionally increased TGF-β1 expression.
Traditional Chinese medicine formulation Yanggan Jiedu Sanjie inhibits TGF-β1-induced epithelial-mesenchymal transition and metastatic potential in human hepatocarcinoma Bel-7402 cells.
Our findings suggest a novel mechanism linking susceptibility to advanced fibrosis and subsequently indirectly to HCC, to the level of MICA expression through TGF-β1-dependent mechanisms.
High plasma level of TGF-β1 in HCC patients up-regulates CD96 expression and dynamically shifts the balance between CD96, TIGIT, and CD226 in NK cells.
123I-scintigraphy revealed significant tumor-specific radioiodide accumulation and thus NIS expression after systemic application of SMAD-NIS-MSCs into mice harboring subcutaneous tumors derived from the human hepatocellular carcinoma (HCC) cell line HuH7, which express TGFB1.
We therefore evaluated the effects of combining focused EBRT (5 Gy) with MSC-mediated systemic delivery of the theranostic <i>NIS</i> transgene under control of a synthetic TGFB1-inducible SMAD-responsive promoter (SMAD-NIS-MSCs) using <sup>123</sup>I-scintigraphy followed by <sup>131</sup>I therapy in CD1 nu/nu mice harboring subcutaneous human hepatocellular carcinoma (HuH7).
The data presented that TGF-β1 and RELN showed an opposite expression pattern, and either increased expression of TGF-β1 or decreased expression of RELN increased HCC cell migration ability.
In conclusion, our study revealed a novel mechanism explaining TGF-β1-induced MDR in HCC through upregulating P-gp and BCRP via the SMAD4/HOTAIR/miR-145 axis.
We assessed the activity of galunisertib, a small molecule inhibitor of the transforming growth factor beta (TGF-β1) receptor I, in second-line patients with hepatocellular carcinoma (HCC) in two cohorts of baseline serum alpha fetoprotein (AFP).
The HCC Hepa1-6 cells were treated with the supernatant of Tregs-conditioned medium (Tregs-CM) to investigate the epithelial-mesenchymal transition (EMT) and TGF-β1.
Furthermore, the number of LAP<sup>+</sup>CD4<sup>+</sup> T cells per high-magnification microscopic field (magnification, ×400) in the HCC tissues was 11.25±3.00, which was significantly higher than that in the peri-cancer tissues (5.75±1.00) and that in the HBV-infected hepatic tissues around benign lesions (2.61±0.83).
SIGNIFICANCE: These findings show that reduced number and function of CD160<sup>+</sup> NK cells in the tumor microenvironment contributes to immune escape of HCC; blocking TGFβ1 restores IFNγ production of CD160<sup>+</sup> NK cells.<b>Graphical Abstract:</b> http://cancerres.aacrjournals.org/content/canres/78/23/6581/F1.large.jpg.
In the current study, we report that GnT-V-mediated N-glycosylation of CD147/basigin, a tumor-associated glycoprotein that carries β1,6-N-acetylglucosamine (β1,6-GlcNAc) glycans, is upregulated during TGF-β1-induced epithelial-to-mesenchymal transition (EMT), which correlates with tumor metastasis in patients with hepatocellular carcinoma (HCC).
Lung fibroblast-conditioned medium stimulated TGF-β1 production from LCCs, whereas LCC-conditioned medium decreased fibroblast survival and α-smooth muscle actin expression by fibroblasts.
In analysis of correlation with tumor stage, both protein and mRNA expression of TGFβ1, Smad1, Smad2 and Smad4 in patients with stage III HCC were significantly lower than those with stage IV HCC (P < 0.001), while the protein and mRNA expression of Smad3 in patients with IV stage HCC was significantly higher in comparison to those with stage IV HCC (P < 0.001).
The clinicopathological features of miR-663a and the correlation between miR-663a and TGF-β1 expression were also investigated in the clinical samples of HCC.
In the present study, transforming growth factor (TGF)‑β1 promoted upregulation of VEGF and downregulation of microRNA (miR)‑20b expression in mouse H22 hepatocellular carcinoma cells. miR‑20b negatively regulated both constitutive VEGF expression and TGF‑β1‑induced VEGF expression.