Evidence map›Paper›PMID 39327674›Full record

ArticleCancer science2024

Selective killing of castration-resistant prostate cancer cells by formycin A via the ATF4-CHOP axis.

Tomoki Takei, Yuki Hamamura, Hiroshi Hongo, Etsu Tashiro, Masaya Imoto, Takeo Kosaka, Mototsugu Oya

Abstract read
In one paragraph

Article in Cancer science, 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
–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

1 citing paper in PubMed.

  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

7 authors.

Tomoki TakeiDepartment of Biosciences and Informatics, Faculty of Science and Technology, Keio University, Yokohama, Japan.
Yuki HamamuraDepartment of Biosciences and Informatics, Faculty of Science and Technology, Keio University, Yokohama, Japan.
Hiroshi HongoDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-3341-1397
Etsu TashiroDepartment of Biosciences and Informatics, Faculty of Science and Technology, Keio University, Yokohama, Japan.ORCID https://orcid.org/0000-0003-4533-623X
Masaya ImotoDepartment of Biosciences and Informatics, Faculty of Science and Technology, Keio University, Yokohama, Japan.ORCID https://orcid.org/0000-0003-4910-3871
Takeo KosakaDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-4371-4594
Mototsugu OyaDepartment of Urology, Keio University School of Medicine, Tokyo, Japan.ORCID https://orcid.org/0000-0002-2048-4263

Funding

Grants-in-Aid for Scientific Research 21K19579Grants-in-Aid for Scientific Research 23K08723Grants-in-Aid for Scientific Research 24K02580
6 · The paper itself

Abstract

Prostate cancer is initially androgen-dependent but often relapses to an androgen-independent state called castration-resistant prostate cancer (CRPC). Currently approved therapies have limited efficacy against CRPC, highlighting the need for novel therapeutic strategies. To address this need, we conducted a drug screen in our previously established aggressive CRPC cell model. We found that formycin A induced cell death in CRPC model cells but not in parental prostate cancer cells. In addition, formycin A upregulated death receptor 5 through the induction of endoplasmic reticulum stress, activating the "extrinsic" apoptosis pathway in CRPC model cells. Moreover, formycin A showed in vivo antitumor efficacy against CRPC xenografts in castrated nude mice. Thus, our findings highlight the potential of formycin A as a CRPC therapeutic.

Indexed as

Activating Transcription Factor 4ApoptosisEndoplasmic Reticulum StressMice, NudeProstatic Neoplasms, Castration-ResistantTranscription Factor CHOPXenograft Model Antitumor AssaysAnimalsCell Line, TumorHumansMaleMiceSignal TransductionActivating Transcription Factor 4ATF4 protein, humanDDIT3 protein, humanTranscription Factor CHOPantitumor activityCRPCdeath receptor 5ER stressformycin A

Identifiers

PMID39327674
PMCPMC11611774

What OpenQuestion holds

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LicenceCC BY-NC
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.