Glucans were also able to lower IL-1β and IL-6 secretion by LPS-activated THP-1/M cells and showed cytotoxic effect on a breast cancer cell line that was not observed on normal breast cells.
The ratios of granulocyte macrophage colony-stimulating factor and interleukin 1β cytokines, produced in tumor, to the expression of CSF2RA and IL1R2 depend on levels of interleukin 6, interleukin 8, tumor necrosis factor α, interferon γ, granulocyte colony-stimulating factor, and vascular endothelial growth factor A and are important factors affecting the progression and metastasis of the breast cancer.
We investigated whether vitamin D receptor (<i>VDR</i>) polymorphisms were associated with cancer biomarkers, i.e., E-cadherin, matrix metallopeptidase 9 (MMP9), interferon β (IFNβ), soluble intercellular adhesion molecule-1 (s-ICAM-1), soluble vascular cell adhesion molecule-1 (s-VCAM-1), tumor necrosis factorα (TNFα), interleukin 6 (IL6), plasminogen activator inhibitor-1(PAI-1), and human high sensitivity C-reactive protein (hs-CRP), among breast cancer survivors who received vitamin D3 supplementation.
The aim of the current study was to assess the effect of coenzyme Q10 supplementation on serum levels of interleukin 6, 8, and vascular endothelial growth factor (VEGF) in patients with breast cancer undergoing tamoxifen therapy by a double-blind, placebo-controlled, randomized clinical trial.
Cytokines such as interleukin-6 (IL-6), oncostatin M (OSM), and interleukin-1 beta (IL-1β) promote the development of both acute and chronic inflammation while promoting <i>in vitro</i> metrics of breast cancer metastasis.
Specifically, IL-6 promoted the proliferation of normal cells and CCL2 induced the M2-like polarization of macrophages, which might create an immunosuppressive microenvironment during the initiation and/or development of breast cancer.
We performed the Wechsler Memory Scale-Revised (WMS-R) test and measured plasma IL-6 levels for 47 breast cancer surgical patients within 1 year after the initial therapy (study 1) and more than 2 years after study 1 (study 2).
Breast cancer cell lines T47D and MCF7 were exposed to IL-6, the expression of PIM1 was examined by quantitative real-time PCR (qRT-PCR) and western blot.
These findings indicate that IL-6 downregulates the tumor suppressor HIC1 and promotes BrCA development in the tumor microenvironment through paracrine or autocrine signaling.
Serum IL-6 level (hazard ratio, 13.230; 95% confidence interval, 1.285-136.214; P=0.030) and triple-negative subtype (hazard ratio, 11.739; 95% confidence interval, 1.415-97.362; P=0.023) were independent prognostic factors for OS, and CRP expression level was an independent prognostic factor for RFS in patients with breast cancer (hazard ratio, 18.571; 95% confidence interval, 2.240-153.949; P=0.007).
We're confused about some data in a recent article entitled "Polymorphic variation in IL-1, IL-6 and IL-10 genes, their circulating serum levels and breast cancer risk in Indian women", which was published online in Cytokine.
These results highlight that the survival of breast cancer patients with high co-expression of VEGF and IL-6 family cytokines is dependent on breast cancer subtype.
Among the isolated compounds, 2 and 5 showed significant inhibitory activities toward the LPS-induced production of IL-6 in the human acute monocytic leukemia cell line THP-1, and 7 displayed cytotoxicity against MCF-7, PC9, A549, and breast cancer stem cells (MCF-7-Oct4-GFP) with IC<sub>50</sub> values of 5.2, 5.6, 7.8, and 10 μM, respectively.
Both the CC chemokine ligand 5 (CCL5/RANTES) and interleukin-6 (IL-6), released by mesenchymal stem cells (MSCs) as well as by neoplastic cells, promote breast cancer cell progression through autocrine and paracrine mechanisms.