Evidence map›Paper›PMID 39964447›Full record

ArticleMedical molecular morphology2025

Vitamin D derivatives inhibit mesenchymal transition of mesothelial cells and mitigate peritoneal dissemination of ovarian cancer.

Kazuhisa Fujita, Maia Hayashi, Masato Yoshihara, Satoshi Nomura, Kazuhisa Kitami, Emiri Miyamoto, Shohei Iyoshi, Kazumasa Mogi, Hiroki Fujimoto, Kaname Uno and 11 more

Abstract read
PubMed Publisher
In one paragraph

Article in Medical molecular morphology, 2025. 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

21 authors.

Kazuhisa Fujita *Department of Obstetrics and Gynecology, Fujita Health University Bantane Hospital, 3-6-10, Otobashi, Nakagawa-ku, Nagoya, Aichi, 454-8509, Japan.
Maia Hayashi *Department of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Masato YoshiharaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan. myoshihara1209@med.nagoya-u.ac.jp.ORCID http://orcid.org/0000-0001-5811-3137
Satoshi NomuraDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Kazuhisa KitamiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Emiri MiyamotoDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Shohei IyoshiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Kazumasa MogiDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Hiroki FujimotoDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Kaname UnoDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Atsushi KunishimaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Yoshihiko YamakitaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Hiroyuki TomitaDepartment of Pathology, Gifu University Graduate School of Medicine, 1-1 Yanagido, Gifu City, 501-1193, Japan.
Rino TsutsumiDepartment of Biotechnology and Life Science, Faculty of Engineering, Tokyo University of Agriculture and Technology, 2-24-16, Naka-cho, Koganei, Tokyo, 184-8588, Japan.
Ryota SakamotoDepartment of Biotechnology and Life Science, Faculty of Engineering, Tokyo University of Agriculture and Technology, 2-24-16, Naka-cho, Koganei, Tokyo, 184-8588, Japan.
Kazuo NagasawaDepartment of Biotechnology and Life Science, Faculty of Engineering, Tokyo University of Agriculture and Technology, 2-24-16, Naka-cho, Koganei, Tokyo, 184-8588, Japan.
Yusuke MasuoLaboratory of Molecular Pharmacotherapeutics, Faculty of Pharmacy, Kanazawa University, Kakuma-Machi, Kanazawa, 920-1192, Japan.
Takumi NishiuchiCenter for Experimental Modeling of Human Disease, Kanazawa University, 13-1 Takaramachi, Kanazawa, Ishikawa, 920-8640, Japan.
Kiyosumi ShibataDepartment of Obstetrics and Gynecology, Fujita Health University Bantane Hospital, 3-6-10, Otobashi, Nakagawa-ku, Nagoya, Aichi, 454-8509, Japan.
Atsushi EnomotoDepartment of Pathology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.
Hiroaki KajiyamaDepartment of Obstetrics and Gynecology, Nagoya University Graduate School of Medicine, 65, Tsuruma-cho, Showa-ku, Nagoya, Aichi, 466-8550, Japan.

Funding

Japan Science and Technology Agency 24013152Japan Society for the Promotion 23K27732Japan Society for the Promotion of Science 21KK0296Japan Society for the Promotion of Science 24K19722
6 · The paper itself

Abstract

Ovarian cancer (OvCa) is a leading cause of gynecological cancer-related mortality, primarily due to peritoneal dissemination, which facilitates metastasis in the abdominal cavity. This study explored the potential of vitamin D and its synthetic derivatives in mitigating peritoneal dissemination by modulating the behavior of mesothelial cells (MCs). Vitamin D, through its receptor (VDR), is known to influence cancer progression, and our findings demonstrate that vitamin D derivatives can inhibit mesenchymal transition of MCs induced by TGF-β1, a key driver of peritoneal dissemination. This study used patient-derived primary MCs and in vivo mouse model to assess the effects of vitamin D derivatives on cell morphology, gene expression, and OvCa cell adhesion. Two vitamin D derivatives, VDR agonist, showed significant efficacy in maintaining epithelial-like MC morphology, reducing TGF-β1-induced changes, and inhibiting OvCa cell adhesion to the peritoneum, similar to calcitriol. Conversely, the VDR antagonist derivative induced MC apoptosis, highlighting the essential role of vitamin D in MC survival. These findings suggest that vitamin D derivatives could serve as promising therapeutic agents for OvCa by preserving peritoneal homeostasis and preventing metastasis. Further research is required to explore a broader range of derivatives and their underlying molecular mechanisms.

Indexed as

Epithelial-Mesenchymal TransitionOvarian NeoplasmsPeritoneal NeoplasmsVitamin DAnimalsApoptosisCell AdhesionCell Line, TumorEpithelial CellsFemaleHumansMicePeritoneumReceptors, CalcitriolTransforming Growth Factor beta1Receptors, CalcitriolTransforming Growth Factor beta1Vitamin DMesenchymal transitionMesothelial cellsOvarian cancerPeritoneal disseminationVitamin D

Identifiers

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.