Evidence map›Paper›PMID 30907484›Full record

ArticleCancer science2019

Serum deprivation-response protein regulates aldehyde dehydrogenase 1 through integrin-linked kinase signaling in endometrioid carcinoma cells.

Shinichiro Tahara, Satoshi Nojima, Kenji Ohshima, Yumiko Hori, Masako Kurashige, Naoki Wada, Yuichi Motoyama, Daisuke Okuzaki, Jun-Ichiro Ikeda, Eiichi Morii

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2019. 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
0.9field-weighted citation impact, top 30% 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, 13 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

10 authors at 1 institution in 1 country.

Shinichiro TaharaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID https://orcid.org/0000-0001-6134-3275
Satoshi NojimaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Kenji OhshimaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yumiko HoriDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Masako KurashigeDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Naoki WadaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Yuichi MotoyamaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Daisuke OkuzakiGenome Information Research Center, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.
Jun-Ichiro IkedaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
Eiichi MoriiDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.
The University of Osaka · JP

Funding

Project MEET, Osaka University Graduate School of MedicineThe Ministry of Education, Culture, Sports, Science and Technology, Japan T16K086490The Ministry of Education, Culture, Sports, Science and Technology, Japan T17K195550The Ministry of Education, Culture, Sports, Science and Technology, Japan T18K070680The Ministry of Education, Culture, Sports, Science and Technology, Japan T18K150780The Ministry of Education, Culture, Sports, Science and Technology, Japan T18K150790The Ministry of Education, Culture, Sports, Science and Technology, Japan T18K151220
6 · The paper itself

Abstract

Endometrioid carcinoma (EC) is one of the most common malignancies of the female genital system. We reported previously that aldehyde dehydrogenase 1 (ALDH1), a predominant isoform of the ALDH family in mammals and a potential marker of normal and malignant stem cells, is related to the tumorigenic potential of EC. We compared the levels of various proteins in human EC cells with high and low ALDH1 expression using shotgun proteomics and found that serum deprivation-response protein (SDPR) was preferentially expressed in cells with high ALDH1 expression. Also known as cavin-2, SDPR is a member of the cavin protein family, which is required for the formation of caveolae. Using SDPR-knockout EC cells generated using the CRISPR/Cas9 system, we revealed that SDPR was correlated with invasion, migration, epithelial-mesenchymal transition, and colony formation, as well as the expression of ALDH1. RNA sequencing showed that integrin-linked kinase (ILK) signaling is involved in the effect of SDPR on ALDH1. Immunohistochemical analysis revealed that the localization of ILK at the cell cortex was disrupted by SDPR knockout, potentially interfering with ILK signaling. Moreover, immunohistochemical analysis of clinical samples showed that SDPR is related to histological characteristics associated with invasiveness, such as poor differentiation, lymphatic invasion, and the microcystic, elongated, and fragmented histopathological pattern. This is, to our knowledge, the first report that SDPR is related to tumor progression.

Indexed as

Aldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyCarcinoma, EndometrioidCarrier ProteinsCell Line, TumorCell MovementCell ProliferationEndometrial NeoplasmsEpithelial-Mesenchymal TransitionFemaleGene Expression Regulation, NeoplasticHumansNeoplasm InvasivenessPhosphate-Binding ProteinsProtein Serine-Threonine KinasesRetinal DehydrogenaseAldehyde DehydrogenaseAldehyde Dehydrogenase 1 FamilyALDH1A1 protein, humanCarrier ProteinsCAVIN2 protein, humanPhosphate-Binding ProteinsProtein Serine-Threonine KinasesRetinal DehydrogenaseScaffold Protein ILKaldehyde dehydrogenase 1endometrioid carcinomaintegrin-linked kinasemicrocystic, elongated and fragmentedserum deprivation-response protein

Identifiers

PMID30907484
PMCPMC6500992
OpenAlexW2935861557

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.