Evidence map›Paper›PMID 36479732›Full record

ArticleCancer science2023

Suppression of androgen receptor signaling induces prostate cancer migration via activation of the CCL20-CCR6 axis.

Hiroshi Kano, Kouji Izumi, Kaoru Hiratsuka, Ren Toriumi, Ryunosuke Nakagawa, Shuhei Aoyama, Taiki Kamijima, Takafumi Shimada, Renato Naito, Suguru Kadomoto and 12 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
1.7field-weighted citation impact, top 15% 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

11 citing papers in PubMed, 12 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. 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

22 authors at 2 institutions in 2 countries.

Hiroshi KanoDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Kouji IzumiDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0002-8480-9100
Kaoru HiratsukaDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Ren ToriumiDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0002-6951-8524
Ryunosuke NakagawaDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0002-2503-8908
Shuhei AoyamaDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Taiki KamijimaDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Takafumi ShimadaDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Renato NaitoDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0002-3936-7235
Suguru KadomotoDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0003-4136-8998
Hiroaki IwamotoDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0003-3599-2217
Hiroshi YaegashiDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0003-3188-8834
Shohei KawaguchiDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.ORCID https://orcid.org/0000-0001-6847-9861
Takahiro NoharaDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Kazuyoshi ShigeharaDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Yoshifumi KadonoDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Yohei SaitoSchool of Pharmaceutical Sciences, College of Medical, Pharmaceutical and Health Science, Kanazawa University, Kanazawa, Japan.
Kyoko Nakagawa-GotoSchool of Pharmaceutical Sciences, College of Medical, Pharmaceutical and Health Science, Kanazawa University, Kanazawa, Japan.
Kazuaki YoshiokaDepartment of Vascular Physiology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Hiroki NakataDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Wen-Jye LinImmunology Research Center, National Health Research Institutes, Miaoli County, Taiwan.
Atsushi MizokamiDepartment of Integrative Cancer Therapy and Urology, Kanazawa University Graduate School of Medical Science, Kanazawa, Japan.
Kanazawa University · JPNational Health Research Institutes · TW

Funding

JSPS KAKENHI 19K09685JSPS KAKENHI 22K09495
6 · The paper itself

Abstract

The suppression of androgen receptor (AR) expression exacerbates the migration potential of prostate cancer. This study identified a previously unrecognized regulation of the AR-controlled pathway that promotes migration potential in prostate cancer cells. Prostate cancer cells that pass through a transwell membrane (mig cells) have a higher migration potential with a decreased AR expression than parental cells. In this study, we aimed to elucidate the mechanism of migration enhancement associated with the suppression of AR signaling. Expression of C-C motif ligand 20 (CCL20) is upregulated in mig cells, unlike in the parental cells. Knockdown of AR with small interfering RNA (siAR) in LNCaP and C4-2B cells increased CCL20 secretion and enhanced the migration of cancer cells. Mig cells, CCL20-treated cells, and siAR cells promoted cell migration with an enhancement of AKT phosphorylation and Snail expression, while the addition of a C-C chemokine receptor 6 (CCR6, the specific receptor of CCL20) inhibitor, anti-CCL20 antibody, and AKT inhibitor suppressed the activation of AKT and Snail. With 59 samples of prostate cancer tissue, CCL20 secretion was profuse in metastatic cases despite low AR expression levels. Snail expression was associated with the expression of CCL20 and CCR6. A xenograft study showed that the anti-CCL20 antibody significantly inhibited Snail expression, thereby suggesting a new therapeutic approach for castration-resistant prostate cancer with the inhibition of the axis between CCL20 and CCR6.

Indexed as

Prostatic NeoplasmsProto-Oncogene Proteins c-aktCell Line, TumorCell ProliferationChemokine CCL20HumansMaleReceptors, AndrogenReceptors, CCR6Signal TransductionCCL20 protein, humanCCR6 protein, humanChemokine CCL20Proto-Oncogene Proteins c-aktReceptors, AndrogenReceptors, CCR6AKTcastration resistantchemokinemigrationSnail

Identifiers

PMID36479732
PMCPMC10067408
OpenAlexW4311927370

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.