This study demonstrates that combined treatment with subtoxic doses of Codium extracts (CE), a flavonoid found in many fruits and vegetables, and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), induces apoptosis in TRAIL-resistant colorectal cancer (CRC) cells.
Further subgroup analyses based on ethnicity of participants revealed that <i>TNF-α</i> -238 G/A was significantly correlated with the risk of CRC in Caucasians (dominant model: <i>P</i> = 0.01, OR = 0.47, 95%CI 0.26-0.86; overdominant model: <i>P</i> = 0.01, OR = 2.27, 95%CI 1.20-4.30; allele model: <i>P</i> = 0.02, OR = 0.51, 95%CI 0.29-0.90), while -308 G/A polymorphism was significantly correlated with the risk of CRC in Asians (recessive model: <i>P</i> = 0.001, OR = 2.23, 95%CI 1.38-3.63).<b>Conclusions:</b> Our findings indicated that <i>TNF-α</i> -238 G/A polymorphism may serve as a potential biological marker for CRC in Caucasians, and <i>TNF-α</i> -308 G/A polymorphism may serve as a potential biological marker for CRC in Asians.
Overall, in this study, we demonstrate that the oncolytic radiotherapy-tumor necrosis factor-related apoptosis-inducing ligand construct can sensitize human colorectal cancer cells to radiation-induced apoptosis both in vitro and in vivo.
<b>Background:</b> This study sought to evaluate the efficacy of a novel intraoperative chemotherapy (IOC) regimen that consists of hydroxycamptothecin, tumor necrosis factor (TNF), 5-fluorouracil (5-FU), and calcium folinate (CF) on the outcomes of colorectal cancer (CRC).
The results also revealed increased levels of P65 and signal transducer and activator of transcription 3 (STAT3) phosphorylation and increased secretion of interleukin‑6 (IL‑6) and tumor necrosis factor‑α (TNF‑α) in CRC tissue compared with levels in precancerous tissue.
Bioinformatics analysis indicated that the 18 herbs realize anti-CRC activity mainly through suppressing the proliferative activity of ERBB2, peroxisome proliferator-activated receptor gamma, and retinoid X receptor, suppressing angiogenesis via inhibition of VEGFR and VEGFA expression, inhibiting the phosphatidylinositol-3-kinase/AKT1 signaling pathway directly through SRC and AKT1, and reducing tumor necrosis factor-induced inflammation.
This study assessed the antitumor effect of circularly permuted tumor necrosis factor-related apoptosis-inducing ligand alone or with 5-fluorouracil in colorectal cancer cells in vitro and explored the underlying mechanisms.
Tumor necrosis factor‑α‑mediated (TNF‑α) epithelial‑mesenchymal transition (EMT) is associated with distant metastasis in patients with colorectal cancer with poor prognosis.
Overexpression of the mitochondrial chaperone tumor necrosis factor receptor-associated protein 1 is associated with the poor prognosis of patients with colorectal cancer.
From a biological perspective, it has been demonstrated that HR2A could have a beneficial effect on CRC for many reasons: i) promotion of peri-tumoral lymphocyte growth and improvement of immune response against the tumor, ii) suppression of adhesion molecules which might favor metastasis, iii) anti-angiogenetic activity (reduction of VEGF), iv) increased production of some cytokines which may counteract tumor growth, such as tumor necrosis factor (TNF) alpha, interleukin (IL)-10 and IL-15.
We used Luminex technology to investigate protein levels of the cytokines IL6, tumor necrosis factor-α (TNFα) and vascular endothelial growth factor (VEGF) to relate these to IL32 levels in CRC tissue.
To explore zinc-α2-glycoprotein (ZAG), leptin, high-molecular-weight adiponectin (HMW-ADPN), and tumor necrosis factor-alpha (TNF-α) levels in serum and subcutaneous and visceral white adipose tissue (sWAT and vWAT) among normal weight (NW) and overweight/obese (OW/OB) patients with colorectal cancer (CRC).
The tumor necrosis factor⁻related weak inducer of apoptosis (TWEAK) belongs to the tumor necrosis factor ligand superfamily, which was shown to play an important role in inflammatory and malignant gastrointestinal diseases, including colitis or colorectal cancer.
Restoration of RUNX1 abolished the inhibitory effects of miR-20a on the secretions of IFN-γ and TNF-α, as well as the killing effect of NK cells to colorectal cancer cells.
Here, we review the current state of knowledge on how obesity affects inflammatory TNFα and IL-6 signaling in hepatocellular carcinoma and colorectal cancers.
Interference of Paxillin significantly decreased Paxillin expression, secretions of IFN-γ and TNF-α, and the killing effect of NK cells to colorectal cancer cells.
We found the concentrations of IL-12(p70), IL-10, IL-1ra, IL-4, IL-6, IL-7, IL-8, G-CSF and TNFα to be significantly higher in right-sided and GM-CSF in left-sided than rectal CRCs.
These results indicate that TNF plays a key role in determining the cytotoxic effectiveness of SN38 in colorectal cancer and suggests a re-evaluation of TNF-based interventions to enhance therapeutic efficacy.<b>Implications:</b> The capacity of RIP1 to influence drug sensitivity suggests RIP1 may have biomarker potential.<i></i>.