Prostaglandin modulates TLR3-induced cytokine expression in human astroglioma cells

Lee, Keimin; Kim, Soo-Jeong; Kim, Dong-Hoon; Jo, Su‐Hyun; Lee, Sung Joong; Choi, Se‐Young

doi:10.1016/j.brainres.2014.06.036

Cited by 6 publications

(3 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Colorectal cancer is the most common malignant tumor and it is estimated there were 1.167 million new cases in 2007 worldwide, ranking third among all malignant tumors; 603,000 succumbed to colorectal cancer in the same year (21,22). Currently, colorectal cancer remains a major threat to human health.…”

Section: Discussionmentioning

confidence: 99%

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway

et al. 2017

View full text Add to dashboard Cite

Abstract.Catalpol is an effective active ingredient that functions as a diuretic and laxative, and exhibits blood sugar-lowering, liver protective, anti-aging and anticancer effects. In traditional Chinese medicine, catalpol is believed to be Yin nourishing. The anticancer effect of catalpol on human HCT116 colorectal cancer cells were investigated and the mechanism of action was evaluated. Cellular viability was detected using an MTT assay. Caspase-3 and caspase-9 activity, cellular apoptosis and nucleic morphology were analyzed using caspase-3 and caspase-9 activity assay kits, flow cytometric assays and DAPI staining assay, respectively. Western blot analysis was used to measure the protein expressions of phosphatidylinositol 3-kinase (PI3K), phosphorylated-protein kinase B (p-Akt) and Akt. Expression of microRNA-200 was detected using the reverse transcription-quantitative polymerase chain reaction. HCT116 cells were incubated with PI3K inhibitors in order to analyze the effect of catalpol on cell proliferation. Catalpol was able to inhibit HCT116 cell proliferation. Furthermore, catalpol induced apoptosis in HCT116 cells, which depended on the increased activities of caspase-3 and -9. In addition, catalpol reduced the expression of PI3K, p-Akt and Akt in HCT116 cells. However, downregulation of PI3K/Akt decreased the viability of HCT116 cells following treatment with catalpol and enhanced microRNA-200 expression. Catalpol promoted cellular apoptosis in human HCT116 colorectal cancer cells through upregulation of microRNA-200 expression, which depended on a downregulation of the phosphatase and tensin homolog/PI3K-Akt signaling pathway.

show abstract

Section: Discussionmentioning

confidence: 99%

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway

et al. 2017

View full text Add to dashboard Cite

show abstract

“…Similar to the induction of pro-inflammatory cytokines, poly(I:C) elicits the secretion of chemokines from GBM cells which can attract tumorlytic lymphocytes. Poly(I:C)/poly-ICLC, targeted to either receptor pathway, stimulates GBM cell secretion of CXCL8, CXCL9, CXCL10, CCL2, CCL4 and CCL5 [ 29 – 34 , 37 – 40 , 45 ]. In transwell assays using supernatant of poly(I:C)-treated pGBM, chemoattraction of CD8 + and CD4 + T cells, but not NK cells, was increased in a manner that suggested involvement of those ligands for CCR5 and CXCR3 [ 30 ].…”

Section: Methodsmentioning

confidence: 99%

A systematic review on poly(I:C) and poly-ICLC in glioblastoma: adjuvants coordinating the unlocking of immunotherapy

Waele

Verhezen

Heijden

et al. 2021

J Exp Clin Cancer Res

View full text Add to dashboard Cite

Immunotherapy is currently under intensive investigation as a potential breakthrough treatment option for glioblastoma. Given the anatomical and immunological complexities surrounding glioblastoma, lymphocytes that infiltrate the brain to develop durable immunity with memory will be key. Polyinosinic:polycytidylic acid, or poly(I:C), and its derivative poly-ICLC could serve as a priming or boosting therapy to unleash lymphocytes and other factors in the (immuno)therapeutic armory against glioblastoma. Here, we present a systematic review on the effects and efficacy of poly(I:C)/poly-ICLC for glioblastoma treatment, ranging from preclinical work on cellular and murine glioblastoma models to reported and ongoing clinical studies. MEDLINE was searched until 15 May 2021 to identify preclinical (glioblastoma cells, murine models) and clinical studies that investigated poly(I:C) or poly-ICLC in glioblastoma. A systematic review approach was conducted according to PRISMA guidelines. ClinicalTrials.gov was queried for ongoing clinical studies. Direct pro-tumorigenic effects of poly(I:C) on glioblastoma cells have not been described. On the contrary, poly(I:C) changes the immunological profile of glioblastoma cells and can also kill them directly. In murine glioblastoma models, poly(I:C) has shown therapeutic relevance as an adjuvant therapy to several treatment modalities, including vaccination and immune checkpoint blockade. Clinically, mostly as an adjuvant to dendritic cell or peptide vaccines, poly-ICLC has been demonstrated to be safe and capable of eliciting immunological activity to boost therapeutic responses. Poly-ICLC could be a valuable tool to enhance immunotherapeutic approaches for glioblastoma. We conclude by proposing several promising combination strategies that might advance glioblastoma immunotherapy and discuss key pre-clinical aspects to improve clinical translation.

show abstract

“…The cAMP concentration in cells was determined using a [ 3 H]cAMP competition assay, evaluating binding to the cAMP‐binding protein . Cells were harvested and preincubated with Locke's solution containing 1 mM isobutylmethyl xanthine (IBMX) to inhibit phosphodiesterase.…”

Section: Methodsmentioning

confidence: 99%

Human salivary gland cells express bradykinin receptors that modulate the expression of proinflammatory cytokines

Lee

Kim

Choi

et al. 2016

European J Oral Sciences

Self Cite

View full text Add to dashboard Cite

Bradykinin is an important peptide modulator that affects the function of neurons and immune cells. However, there is no evidence of the bradykinin receptors and their functions in human salivary glands. Here we have identified and characterized bradykinin receptors on human submandibular gland cells. Both bradykinin B1 and B2 receptors are expressed on human submandibular gland cells, A253 cells, and HSG cells. Bradykinin increased the intracellular Ca concentration ([Ca ] ) in a concentration-dependent manner. Interestingly, a specific agonist of the B1 receptor did not have any effect on [Ca ] in HSG cells, whereas specific agonists of the B2 receptor had a Ca mobilizing effect. Furthermore, application of the B1 receptor antagonist, R715, did not alter the bradykinin-mediated increase in cytosolic Ca , whereas the B2 receptor antagonist, HOE140, showed a strong inhibitory effect, which implies that bradykinin B2 receptors are functional in modulating the concentration of cytosolic Ca . Bradykinin did not affect a carbachol-induced rise of [Ca ] and did not modulate translocation of aquaporin-5. However, bradykinin did promote the expression of proinflammatory cytokines, including tumor necrosis factor-α (TNF-α), implying the role of bradykinin in salivary gland inflammation. These data suggest that bradykinin receptors are involved in Ca signaling in human submandibular gland cells and serve a unique role, which is separate from that of other salivary gland G protein-coupled receptors.

show abstract

Prostaglandin modulates TLR3-induced cytokine expression in human astroglioma cells

Cited by 6 publications

References 39 publications

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway

Catalpol promotes cellular apoptosis in human HCT116 colorectal cancer cells via microRNA-200 and the downregulation of PI3K-Akt signaling pathway

A systematic review on poly(I:C) and poly-ICLC in glioblastoma: adjuvants coordinating the unlocking of immunotherapy

Human salivary gland cells express bradykinin receptors that modulate the expression of proinflammatory cytokines

Contact Info

Product

Resources

About