Tumor necrosis factor receptor-associated factor 5 (TRAF5) was a neighboring gene of LINC00467 and its expression was positively modulated by LINC00467 in HCC.
Besides, examination of HCC clinical samples demonstrated that IL-6 and TNF-α production correlated with HPC activation, hepatic fibrosis, and HCC recurrence.
Of note, the TPG-1 treatment significantly inhibited the tumorigenesis of human hepatoma HepG2 cells likely at least in part by increasing serum levels of TNFα and promoting leukocyte infiltration into tumors in nude mice.
A significant decrease in the frequency of TNFα producing FcεRI<sup>+</sup> monocytes and mDCs in HCC and CCA patients when compared to the group of healthy individuals was observed, and a close association between FcεRI<sup>+</sup> monocytes and mDCs dysfunction was identified.
Whole blood was obtained for analysis of T cell cytokines (IL-1β, IL-2, IL-4, IL-5, IL-6, IL-9, IL-10, IL-12p70, IL-13, IL-17A, IL-22, IFN-γ, and TNF-α) and Tregs from 142 HCC patients.
Here, using immunoblotting analyses and various molecular genetic approaches in HepG2 and SMMC-7721 cells, we demonstrate that GADD34 protects hepatocellular carcinoma (HCC) cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by stabilizing a BCL-2 family member, myeloid cell leukemia 1 (MCL-1).
TNF-α derived from M2 tumor-associated macrophages promotes epithelial-mesenchymal transition and cancer stemness through the Wnt/β-catenin pathway in SMMC-7721 hepatocellular carcinoma cells.
It was revealed as significant downregulation of the mRNA expression levels of nuclear factor-kappa B and tumor necrosis factor α as well as suppression of Ki-67 protein expression level in diethylnitrosamine (DEN)-induced HCC mice (<i>P</i> < 0.05).
The inflammatory cytokines tumor necrosis factor-α and interleukin-6 and their downstream targets nuclear factor kappa B (NF-κB), c-Jun N-terminal kinase (JNK), and signal transducer and activator of transcription 3 drive inflammation-associated HCC.
The present study confirmed that high preoperative serum IL6, IL8, and TNF-<i>α</i> levels were distinctly correlated with the postoperative tumor recurrence risk of HCC patients.
Additionally, multivariate Cox regression models suggested that high expression levels of TNF-α alone, p38MAPK alone, or TNF-α and p38MAPK together in the HCC microenvironment were independent predictive factors for OS and DFS rates (P<0.05).
To investigate the effects of angiotensin II (Ang II) and tumor necrosis factor-α (TNF-α) on the biological characteristics of hepatocellular carcinoma (HCC) cells and the associated changes in G protein-coupled receptor kinase 2 (GRK2) expression.
Interestingly, treatment with GME elicited marked improvement in the liver histological feature and downregulation of tumor necrosis factor-alpha levels in HCC groups.
Adipose tissue is regarded as an endocrine organ that secretes proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6), which are related to the progression of hepatocellular carcinoma (HCC).
As well, reduced triglyceride (TG), total cholesterol (T-CHOL), interferon gamma (IFN-γ), and tumor necrosis factor alpha (TNF-α) levels in sera were checked in Sor-treated HCC patients.
Evidence has shown that most hepatocellular carcinoma (HCC) cells are resistant to tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL)-mediated apoptosis.
We report here that DDIAS protects cancer cells from tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by two distinct mechanisms in non-small cell lung cancer (NSCLC) and hepatocellular carcinoma (HCC) cells.