Evidence map›Paper›PMID 38478219›Full record

ArticlePharmacological reports : PR2024

Transcriptome analysis of an AKT inhibitor-resistant endometrial cancer cell line.

Takafumi Onishi, Tsuyoshi Takashima, Kazuki Shibahara, Shoji Takagi, Shinichi Tanaka, Michihiro Mori, Hirokazu Odashima, Yukihiko Osawa, Manabu Hattori

Abstract read
PubMed Publisher
In one paragraph

Article in Pharmacological reports : PR, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

1 citing paper in PubMed, 2 citations in OpenAlex.

  1. Article
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

9 authors at 6 institutions in 1 country.

Takafumi OnishiDepartment of Medical Technology and Sciences, Faculty of Health Sciences, Kyoto Tachibana University, 34 Yamada-cho, Oyake, Yamashina-ku, Kyoto, 607-8175, Japan. onishi-ta@tachibana-u.ac.jp.ORCID http://orcid.org/0000-0002-2494-1265
Tsuyoshi TakashimaDepartment of Pathology, Osaka University Graduate School of Medicine, Osaka, Japan.ORCID http://orcid.org/0000-0003-1362-3883
Kazuki ShibaharaDepartment of Medical Life Sciences, School of Medical Life Sciences, Kyushu University of Health and Welfare, Miyazaki, Japan.ORCID http://orcid.org/0009-0003-7060-5857
Shoji TakagiDepartment of Medical Life Science, College of Life Science, Kurashiki University of Science and the Arts, Okayama, Japan.ORCID http://orcid.org/0009-0006-0643-9323
Shinichi TanakaDepartment of Medical Technology, Kawasaki University of Medical Welfare, Okayama, Japan.ORCID http://orcid.org/0000-0003-1723-9459
Michihiro MoriDepartment of Health and Nutrition, Faculty of Health Science, Kio University, Nara, Japan.ORCID http://orcid.org/0000-0002-4375-2670
Hirokazu OdashimaDepartment of Medical Technology and Sciences, Faculty of Health Sciences, Kyoto Tachibana University, 34 Yamada-cho, Oyake, Yamashina-ku, Kyoto, 607-8175, Japan.
Yukihiko OsawaDepartment of Medical Technology and Sciences, Faculty of Health Sciences, Kyoto Tachibana University, 34 Yamada-cho, Oyake, Yamashina-ku, Kyoto, 607-8175, Japan.
Manabu HattoriDepartment of Medical Technology and Sciences, Faculty of Health Sciences, Kyoto Tachibana University, 34 Yamada-cho, Oyake, Yamashina-ku, Kyoto, 607-8175, Japan.
Kyoto Tachibana University · JPKawasaki University of Medical Welfare · JPKio University · JPKurashiki University of Science and the Arts · JPKyushu University of Health and Welfare · JPThe University of Osaka · JP

Funding

Kyoto Tachibana university 23007
6 · The paper itself

Abstract

backgroundDrug resistance in endometrial cancer (EC) is a serious problem and a barrier to improving prognosis. The PI3K/AKT/mTOR pathway is highly activated in EC and can serve as a potential therapeutic target. Inhibitors against AKT have been developed, but resistance to these inhibitors is a concern. This study aimed to establish AKT inhibitor resistant cell lines and identify differentially expressed genes (DEGs) between parental and AKT inhibitor resistant cell lines to understand the mechanism of drug resistance to AKT inhibitors in EC.

methodsThe sensitivity of eight EC cell lines to AKT inhibitor was analyzed. One of them was used to establish a drug-resistant cell line. DEGs were examined using RNA sequencing (RNA-seq). Furthermore, DEGs were comprehensively analyzed to identify hub genes. Hub genes were evaluated using quantitative real-time polymerase chain reaction.

resultsRNA-seq identified 617 DEGs. Hub genes were selected using bioinformatics analysis. The top 10 hub genes were TNF, CDH1, CCND1, COL1A1, CDH2, ICAM1, CAV1, THBS1, NCAM1, and CDKN2A. Relative mRNA expression was significantly upregulated for TNF, CDH1, CCND1, THBS1, p16

conclusionsDrug resistance to AKT inhibitors may depend on genes related to cell adhesion-mediated resistance and transforming growth factor β signaling.

Indexed as

Endometrial NeoplasmsProto-Oncogene Proteins c-aktCell Line, TumorFemaleGene Expression ProfilingHumansPhosphatidylinositol 3-KinasesProtein Kinase InhibitorsTranscriptomePhosphatidylinositol 3-KinasesProtein Kinase InhibitorsProto-Oncogene Proteins c-aktAKT inhibitorBorussertibCell adhesion-mediated drug resistanceDrug resistanceEndometrial cancerTGF-β signaling

Identifiers

PMID38478219
OpenAlexW4392744661

What OpenQuestion holds

Textmetadata
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.