ArticleOncology letters2015
JAK/STAT3 signaling pathway mediates endothelial-like differentiation of immature dendritic cells.
Article in Oncology letters, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- Axon Regeneration: A Subcellular Extension in Multiple Dimensions.Cold Spring Harbor perspectives in biology · 2022Review
- Anti-Inflammatory and Immunoregulatory Action of Sesquiterpene Lactones.Molecules (Basel, Switzerland) · 2022Review
- Significance of STAT3 in Immune Infiltration and Drug Response in Cancer.Biomolecules · 2020Article
- Monocyte-Derived Dendritic Cell Differentiation in Inflammatory Arthritis Is Regulated by the JAK/STAT Axis via NADPH Oxidase Regulation.Frontiers in immunology · 2020Article
- Combination curcumin and (-)-epigallocatechin-3-gallate inhibits colorectal carcinoma microenvironment-induced angiogenesis by JAK/STAT3/IL-8 pathway.Oncogenesis · 2017Article
- Metformin inhibits esophageal squamous cell carcinoma-induced angiogenesis by suppressing JAK/STAT3 signaling pathway.Oncotarget · 2017Article
- Dendritic cells loading autologous tumor lysate promote tumor angiogenesis.Tumour biology : the journal of the International Society for Oncodevelopmental Biology and Medicine · 2016Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Endothelial-like differentiation (ELD) of dendritic cells (DCs) is a poorly understood phenomenon. The present study evaluated the effect on the ELD of DCs by using human esophageal squamous cell carcinoma (ESCC) cells with high or poor differentiation. The results demonstrated that KYSE450 (highly differentiated) and KYSE70 (poorly differentiated) cell supernatants induce the differentiation of immature DCs (iDCs), derived from healthy adult volunteers, away from the DC pathway and towards an endothelial cell (EC) fate. This effect was strongest in the cells treated with the KYSE70 supernatant. During the ELD of iDCs, sustained activation of JAK (janus tyrosine kinase)/STAT3 (signal transducer and activator of transcription 3) signaling was detected. Incubation of iDCs with the JAK inhibitor, AG490 blocked JAK/STAT3 phosphorylation and iDC differentiation. These results suggested that the JAK/STAT3 signaling pathway mediates ELD of iDCs. Furthermore, the poorly differentiated ESCC cells may have a greater effect on the ELD of iDCs than highly differentiated ESCC cells.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.