Evidence map›Paper›PMID 28178391›Full record

ArticleCancer science2017

Amino-terminal enhancer of split gene AES encodes a tumor and metastasis suppressor of prostate cancer.

Yoshiyuki Okada, Masahiro Sonoshita, Fumihiko Kakizaki, Naoki Aoyama, Yoshiro Itatani, Masayuki Uegaki, Hiromasa Sakamoto, Takashi Kobayashi, Takahiro Inoue, Tomomi Kamba and 3 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.4field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 15 citations in OpenAlex.

  1. Article
  2. Bmal1 Regulates Prostate Growth via Cell-Cycle Modulation.International journal of molecular sciences · 2022
    Article
  3. Article
  4. Frontiers in oncology · 2022
    Review
  5. Review
  6. Review
  7. Article
  8. A strategy for the identification of paracrine regulators of cancer cell migration.Clinical and experimental pharmacology & physiology · 2020
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

13 authors at 2 institutions in 1 country.

Yoshiyuki OkadaDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masahiro SonoshitaDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Fumihiko KakizakiDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Naoki AoyamaDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yoshiro ItataniDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Masayuki UegakiDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Hiromasa SakamotoDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takashi KobayashiDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Takahiro InoueDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Tomomi KambaDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Akira SuzukiDivision of Cancer Genetics, Medical Institute of Bioregulation, Kyushu University, Fukuoka, Japan.
Osamu OgawaDepartment of Urology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
M Mark TaketoDepartment of Pharmacology, Kyoto University Graduate School of Medicine, Kyoto, Japan.ORCID http://orcid.org/0000-0002-9032-4505
Kyoto University · JPKyushu University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

A major cause of cancer death is its metastasis to the vital organs. Few effective therapies are available for metastatic castration-resistant prostate cancer (PCa), and progressive metastatic lesions such as lymph nodes and bones cause mortality. We recently identified AES as a metastasis suppressor for colon cancer. Here, we have studied the roles of AES in PCa progression. We analyzed the relationship between AES expression and PCa stages of progression by immunohistochemistry of human needle biopsy samples. We then performed overexpression and knockdown of AES in human PCa cell lines LNCaP, DU145 and PC3, and determined the effects on proliferation, invasion and metastasis in culture and in a xenograft model. We also compared the PCa phenotypes of Aes/Pten compound knockout mice with those of Pten simple knockout mice. Expression levels of AES were inversely correlated with clinical stages of human PCa. Exogenous expression of AES suppressed the growth of LNCaP cells, whereas the AES knockdown promoted it. We also found that AES suppressed transcriptional activities of androgen receptor and Notch signaling. Notably, AES overexpression in AR-defective DU145 and PC3 cells reduced invasion and metastasis to lymph nodes and bones without affecting proliferation in culture. Consistently, prostate epithelium-specific inactivation of Aes in Pten

Indexed as

AgedAnimalsBlotting, WesternCell Line, TumorCell MovementCo-Repressor ProteinsHumansImmunohistochemistryMaleMiceMice, Inbred C57BLMice, Inbred NODMice, KnockoutMice, NudeMice, SCIDMice, TransgenicCo-Repressor ProteinsPTEN PhosphohydrolaseReceptors, AndrogenReceptors, NotchRepressor ProteinsTLE5 protein, humanTumor Suppressor ProteinsAndrogen receptorsneoplasm invasivenessneoplasm metastasisprostatic neoplasmstranscription factors

Identifiers

PMID28178391
PMCPMC5406606
OpenAlexW2586906027

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.