Evidence map›Paper›PMID 38250514›Full record

ArticlePNAS nexus2024

G-protein signaling of oxytocin receptor as a potential target for cabazitaxel-resistant prostate cancer.

Hiroshi Hongo, Takeo Kosaka, Ken-Ichi Takayama, Yuto Baba, Yota Yasumizu, Koji Ueda, Yutaka Suzuki, Satoshi Inoue, Himisha Beltran, Mototsugu Oya

Open access · goldAbstract read
In one paragraph

Article in PNAS nexus, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.6field-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

3 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
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 5 institutions in 2 countries.

Hiroshi HongoDepartment of Urology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.ORCID https://orcid.org/0000-0002-3341-1397
Takeo KosakaDepartment of Urology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.ORCID https://orcid.org/0000-0002-4371-4594
Ken-Ichi TakayamaDepartment of Systems Aging Science and Medicine, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo 173-001, Japan.ORCID https://orcid.org/0000-0002-2832-1434
Yuto BabaDepartment of Urology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.
Yota YasumizuDepartment of Urology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.ORCID https://orcid.org/0000-0002-1725-6454
Koji UedaCancer Proteomics Group, Cancer Precision Medicine Center, Japanese Foundation for Cancer Research, Koto-ku, Tokyo 135-8550, Japan.ORCID https://orcid.org/0000-0001-9066-4959
Yutaka SuzukiDepartment of Computational Biology and Medical Sciences, Graduate School of Frontier Sciences, The University of Tokyo, Chiba 277-8562, Japan.ORCID https://orcid.org/0000-0003-4852-1879
Satoshi InoueDepartment of Systems Aging Science and Medicine, Tokyo Metropolitan Institute of Gerontology, Itabashi-ku, Tokyo 173-001, Japan.
Himisha BeltranDepartment of Medical Oncology, Dana Farber Cancer Institute, Boston, MA 02215, USA.ORCID https://orcid.org/0000-0003-3259-2226
Mototsugu OyaDepartment of Urology, Keio University School of Medicine, Shinjuku-ku, Tokyo 160-8582, Japan.
Keio University · JPTokyo Metropolitan Institute of Gerontology · JPHarvard University · USJapanese Foundation For Cancer Research · JPThe University of Tokyo · JP

Funding

Molecular mechanisms underlying lineage plasticity in prostate cancerR37CA241486 · NCI · DANA-FARBER CANCER INST · PI Himisha Beltran · 2020 to 2026
$4.1M
NCI NIH HHS R37 CA241486
6 · The paper itself

Abstract

Although the treatment armamentarium for patients with metastatic prostate cancer has improved recently, treatment options after progression on cabazitaxel (CBZ) are limited. To identify the mechanisms underlying CBZ resistance and therapeutic targets, we performed single-cell RNA sequencing of circulating tumor cells (CTCs) from patients with CBZ-resistant prostate cancer. Cells were clustered based on gene expression profiles. In silico screening was used to nominate candidate drugs for overcoming CBZ resistance in castration-resistant prostate cancer. CTCs were divided into three to four clusters, reflecting intrapatient tumor heterogeneity in refractory prostate cancer. Pathway analysis revealed that clusters in two cases showed up-regulation of the oxytocin (OXT) receptor-signaling pathway. Spatial gene expression analysis of CBZ-resistant prostate cancer tissues confirmed the heterogeneous expression of OXT-signaling molecules. Cloperastine (CLO) had significant antitumor activity against CBZ-resistant prostate cancer cells. Mass spectrometric phosphoproteome analysis revealed the suppression of OXT signaling specific to CBZ-resistant models. These results support the potential of CLO as a candidate drug for overcoming CBZ-resistant prostate cancer via the inhibition of OXT signaling.

Indexed as

cabazitaxel-resistant prostate cancerG-protein signalingoxytocin

Identifiers

PMID38250514
PMCPMC10799637
OpenAlexW4390577801

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.