Detail of Figure1A_control_MDCK_CNO

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Project
Title
Live imaging of MDCK cells expressing the PKA biosensor after CNO treatment in control
Description
Live imaging of MDCK cells expressing the PKA biosensor after CNO treatment in control
Release, Updated
2023-02-21
License
CC-BY
Kind
Image data
File Formats
uncompressed TIFF
Data size
2.0 GB

Organism
Canis lupus familiaris ( NCBITaxon:9615 )
Strain(s)
-
Cell Line
MDCK cell ( CLO_0007646 )
Protein names
PKA

Datatype
-
Molecular Function (MF)
G protein-coupled receptor binding ( GO:0001664 )
Biological Process (BP)
Cellular Component (CC)
Biological Imaging Method
time lapse microscopy ( Fbbi:00000249 )
X scale
0.638924 micrometer/pixel
Y scale
0.638924 micrometer/pixel
Z scale
-
T scale
15 sec per time interval

Image Acquisition
Experiment type
-
Microscope type
-
Acquisition mode
-
Contrast method
-
Microscope model
-
Detector model
-
Objective model
-
Filter set
-

Summary of Methods
See details in Konishi Y, et. al. (2021) Cancer Res, 2021 Aug 1;81(15):4124-4132.
Related paper(s)

Yoshinobu Konishi, Hiroshi Ichise, Tetsuya Watabe, Choji Oki, Shinya Tsukiji, Yoko Hamazaki, Yasuhiro Murakawa, Akifumi Takaori-Kondo, Kenta Terai, Michiyuki Matsuda (2021) Intravital Imaging Identifies the VEGF-TXA2 Axis as a Critical Promoter of PGE2 Secretion from Tumor Cells and Immune Evasion., Cancer research, Volume 81, Number 15, pp. 4124-4132

Published in 2021 Aug 1 (Electronic publication in May 25, 2021, midnight )

(Abstract) Prostaglandin E2 (PGE2) promotes tumor progression through evasion of antitumor immunity. In stark contrast to cyclooxygenase-dependent production of PGE2, little is known whether PGE2 secretion is regulated within tumor tissues. Here, we show that VEGF-dependent release of thromboxane A2 (TXA2) triggers Ca(2+) transients in tumor cells, culminating in PGE2 secretion and subsequent immune evasion in the early stages of tumorigenesis. Ca(2+) transients caused cPLA2 activation and triggered the arachidonic acid cascade. Ca(2+) transients were monitored as the surrogate marker of PGE2 secretion. Intravital imaging of Braf(V600E) mouse melanoma cells revealed that the proportion of cells exhibiting Ca(2+) transients is markedly higher in vivo than in vitro. The TXA2 receptor was indispensable for the Ca(2+) transients in vivo, high intratumoral PGE2 concentration, and evasion of antitumor immunity. Notably, treatment with a VEGF receptor antagonist and an anti-VEGF antibody rapidly suppressed Ca(2+) transients and reduced TXA2 and PGE2 concentrations in tumor tissues. These results identify the VEGF-TXA2 axis as a critical promoter of PGE2-dependent tumor immune evasion, providing a molecular basis underlying the immunomodulatory effect of anti-VEGF therapies. SIGNIFICANCE: This study identifies the VEGF-TXA2 axis as a potentially targetable regulator of PGE2 secretion, which provides novel strategies for prevention and treatment of multiple types of malignancies.
(MeSH Terms)

Contact
Kenta Terai , kyoto University , Graduate School of Medicine , Department of Pathology and Biology of Diseases
Contributors

OMERO Dataset
OMERO Project
Source