Evidence map›Paper›PMID 36854451›Full record

ArticleCancer science2023

Cancer cell-derived CD69 induced under lipid and oxygen starvation promotes ovarian cancer progression through fibronectin.

Shiro Koizume, Tomohiko Kanayama, Yayoi Kimura, Hisashi Hirano, Tomoko Takahashi, Yukihide Ota, Kaoru Miyazaki, Mitsuyo Yoshihara, Yoshiyasu Nakamura, Tomoyuki Yokose and 6 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

7 citing papers in PubMed, 8 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

16 authors at 3 institutions in 1 country.

Shiro KoizumeMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.ORCID https://orcid.org/0000-0002-9132-5286
Tomohiko KanayamaMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Yayoi KimuraAdvancer Medical Research Center, Yokohama City University, Yokohama, Japan.
Hisashi HiranoAdvancer Medical Research Center, Yokohama City University, Yokohama, Japan.
Tomoko TakahashiMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Yukihide OtaMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Kaoru MiyazakiMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.ORCID https://orcid.org/0000-0002-2831-2183
Mitsuyo YoshiharaMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Yoshiyasu NakamuraMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Tomoyuki YokoseDepartment of Pathology, Kanagawa Cancer Center Hospital, Yokohama, Japan.
Hisamori KatoDepartment of Gynecology, Kanagawa Cancer Center Hospital, Yokohama, Japan.
Katsuya TakenakaMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Shinya SatoMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.ORCID https://orcid.org/0000-0002-2155-2379
Hiroko TadokoroMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Etsuko MiyagiDepartment of Obstetrics, Gynecology and Molecular Reproductive Science, Yokohama City University Graduate School of Medicine, Yokohama, Japan.
Yohei MiyagiMolecular Pathology and Genetics Division, Kanagawa Cancer Center Research Institute, Yokohama, Japan.
Kanagawa Prefectural Hospital Organization · JPYokohama City University Medical Center · JPYokohama City University · JP

Funding

JSPS KAKENHI 25830097JSPS KAKENHI JP16H06277JSPS KAKENHI JP22H04923
6 · The paper itself

Abstract

Cancer tissues generally have molecular oxygen and serum component deficiencies because of poor vascularization. Recently, we revealed that ICAM1 is strongly activated through lipophagy in ovarian clear cell carcinoma (CCC) cells in response to starvation of long-chain fatty acids and oxygen and confers resistance to apoptosis caused by these harsh conditions. CD69 is a glycoprotein that is synthesized in immune cells and is associated with their activation through cellular signaling pathways. However, the expression and function of CD69 in nonhematological cells is unclear. Here, we report that CD69 is induced in CCC cells as in ICAM1. Mass spectrometry analysis of phosphorylated peptides followed by pathway analysis revealed that CD69 augments CCC cell binding to fibronectin (FN) in association with the phosphorylation of multiple cellular signaling molecules including the focal adhesion pathway. Furthermore, CD69 synthesized in CCC cells could facilitate cell survival because the CD69-FN axis can induce epithelial-mesenchymal transition. Experiments with surgically removed tumor samples revealed that CD69 is predominantly expressed in CCC tumor cells compared with other histological subtypes of epithelial ovarian cancer. Overall, our data suggest that cancer cell-derived CD69 can contribute to CCC progression through FN.

Indexed as

FibronectinsOvarian NeoplasmsCell Line, TumorFemaleHumansLipidsOxygenSignal TransductionFibronectinsLipidsOxygenCD69epithelial-mesenchymal transitionhypoxialipid metabolismtumor microenvironment

Identifiers

PMID36854451
PMCPMC10236627
OpenAlexW4322621651

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

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.