ArticlePloS one2019
B7-1 drives TGF-β stimulated pancreatic carcinoma cell migration and expression of EMT target genes.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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.
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Who cites it
8 citing papers in PubMed, 23 citations in OpenAlex.
- Research progress of CD80 in the development of immunotherapy drugs.Frontiers in immunology · 2024Review
- Gefitinib enhances the anti‑tumor immune response against EGFR‑mutated NSCLC by upregulating B7H5 expression and activating T cells via CD28H.International journal of oncology · 2022Article
- HHLA2 promotes tumor progression by long non‑coding RNA H19 in human gallbladder cancer.International journal of oncology · 2022Article
- Correlation of elastic characteristics of breast lesions with the expression of Smad2/3.Annals of translational medicine · 2021Article
- TGFβ Signaling in the Pancreatic Tumor Microenvironment.Cancers · 2021Review
- Inhibition of TGF-β2-induced migration and epithelial-mesenchymal transition in ARPE-19 by sulforaphane.International journal of ophthalmology · 2021Article
- Immune checkpoint molecules are regulated by transforming growth factor (TGF)-International journal of medical sciences · 2021Article
- EVI5 is an oncogene that regulates the proliferation and metastasis of NSCLC cells.Journal of experimental & clinical cancer research : CR · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
B7-1 proteins are routinely expressed on the surface of antigen presenting cells (APC) and within the innate immune system. They function to establish a biologically optimal and dynamic balance between immune activation and inhibition or self-tolerance. Interactions between B7-1 and its receptors, which include CD28, CTLA4 and PD-L1, contribute to both stimulatory as well as inhibitory or homeostatic regulation. In the current study, we investigated whether the tumor-promoting actions of transforming growth factor beta (TGF-β) disrupted this equilibrium in pancreatic cancer to promote malignant progression and an enhanced means to evade immune detection. The data show that B7-1 is (i) upregulated following treatment of pancreatic carcinoma cells with TGF-β; (ii) induced by TGF-β via both Smad2/3-dependent and independent pathways; (iii) required for pancreatic tumor cell in vitro migration/invasion; and (iv) necessary for TGF-β regulated epithelial-mesenchymal transition (EMT) through induction of Snail family members. Results from the proposed studies provide valuable insights into mechanisms whereby TGF-β regulates both the innate immune response and intrinsic properties of pancreatic tumor growth.
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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.