Evidence map›Paper›PMID 41869454›Full record

ArticleJournal of Cancer2026

FBXW7 suppresses cell proliferation, migration, and epithelial-mesenchymal transition in endometrioid ovarian carcinoma.

Ching-Chou Tsai, Chia-Yi Hsu, Jau-Ling Suen, Hung-Pin Tu, Kun-Bow Tsai, Shun-Chen Huang, Yu-Che Ou, Eing-Mei Tsai

Abstract read
In one paragraph

Article in Journal of Cancer, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

8 authors.

Ching-Chou TsaiGraduate Institute of Clinical Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung City 807, Taiwan.
Chia-Yi HsuGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung City 807, Taiwan.
Jau-Ling SuenGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung City 807, Taiwan.
Hung-Pin TuDepartment of Public Health and Environmental Medicine, School of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 807, Taiwan.
Kun-Bow TsaiDepartment of Pathology, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung City, Taiwan.
Shun-Chen HuangDepartment of Anatomic Pathology, Kaohsiung Chang Gung Memorial Hospital and Chang Gung University, Kaohsiung 833, Taiwan.
Yu-Che OuDepartment of Obstetrics and Gynecology, Chia-Yi Chang Gung Memorial Hospital, Chia-Yi 613, Taiwan.
Eing-Mei TsaiGraduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung City 807, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial ovarian carcinoma is a common gynecologic malignancy. Evidence from several studies suggests that subtypes of this cancer-specifically clear-cell ovarian carcinoma and endometrioid ovarian carcinoma (ENOC)-are associated with endometriosis. FBXW7 (F-box and WD repeat domain containing 7) is a tumor suppressor and component of an E3 ubiquitin ligase complex, which is responsible for tagging proteins for proteasomal degradation. FBXW7 is one of the most frequently dysregulated proteins of the ubiquitin-proteasome system in various human cancers. Thus, we investigated whether FBXW7 dysfunction contributes to epithelial ovarian carcinoma. We found that the level of FBXW7 was lower in endometriosis-associated ovarian carcinoma, especially ENOC. Functional assays revealed that overexpression of FBXW7 inhibited the proliferation and migration of ovarian carcinoma cells, whereas FBXW7 knockdown had the opposite effect. We also found that FBXW7 expression was associated with reduced vimentin levels, accompanied by changes in epithelial-mesenchymal transition (EMT) markers. Overexpression of FBXW7 increased E-cadherin levels while reducing N-cadherin and vimentin levels, thereby promoting the epithelial phenotype. Conversely, FBXW7 knockdown upregulated vimentin and N-cadherin levels, facilitating EMT. Co-immunoprecipitation assays indicated that FBXW7 co-precipitates with vimentin, suggesting a possible role for FBXW7 in influencing vimentin abundance. These findings highlight FBXW7 as a potential tumor suppressor in endometriosis-associated ovarian carcinoma, with effect on cell proliferation, migration, and EMT regulation. The FBXW7-vimentin association may represent previously unrecognized pathway with therapeutic relevance in ovarian carcinoma.

Indexed as

endometrioid ovarian carcinomaepithelial-mesenchymal transitionepithelial ovarian carcinomaFBXW7

Identifiers

PMID41869454
PMCPMC13003548

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.