Evidence map›Paper›PMID 36794010›Full record

ArticleFood & nutrition research2023

Inhibition of castration-resistant prostate cancer growth by genistein through suppression of AKR1C3.

Xiaoping Yu, Jiali Yan, Yulu Li, Jing Cheng, Lujie Zheng, Tianyu Fu, Yanfeng Zhu

Open access · goldAbstract read
In one paragraph

Article in Food & nutrition research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

15 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Molecular Pathways of Genistein Activity in Breast Cancer Cells.International journal of molecular sciences · 2024
    Review
  10. Review
  11. Review
  12. Article
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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 at 3 institutions in 1 country.

Xiaoping YuSchool of Medicine and Nursing, Chengdu University, Chengdu, China.
Jiali YanSchool of Public Health, Chengdu Medical College, Chengdu, China.
Yulu LiNational Institute for Occupational Health and Poison Control, Chinese Center for Disease Control and Prevention, Beijing, China.
Jing ChengSchool of Public Health, Chengdu Medical College, Chengdu, China.
Lujie ZhengSchool of Public Health, Chengdu Medical College, Chengdu, China.
Tianyu FuSchool of Public Health, Chengdu Medical College, Chengdu, China.
Yanfeng ZhuSchool of Public Health, Chengdu Medical College, Chengdu, China.
Chengdu Medical College · CNChengdu University · CNNational Institute for Occupational Health and Poison Control · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Prostate cancer is the second leading cause of cancer-related death among males in America. The patients' survival time is significantly reduced after prostate cancer develops into castration-resistant prostate cancer (CRPC). It has been reported that AKR1C3 is involved in this progression, and that its abnormal expression is directly correlated with the degree of CRPC malignancy. Genistein is one of the active components of soy isoflavones, and many studies have suggested that it has a better inhibitory effect on CRPC. Objective: This study aimed to investigate the antitumor effect of genistein on CRPC and the potential mechanism of action. Design: A xenograft tumor mouse model established with 22RV1 cells was divided into the experimental group and the control group, and the former was given 100 mg/kg.bw/day of genistein, with 22RV1, VCaP, and RWPE-1 cells cultured in a hormone-free serum environment and treated with different concentrations of genistein (0, 12.5, 25, 50, and 100 μmol/L) for 48 h. Molecular docking was used to elucidate the molecular interactions between genistein and AKR1C3. Results: Genistein inhibits CRPC cell proliferation and in vivo tumorigenesis. The western blot analysis confirmed that the genistein significantly inhibited prostate-specific antigen production in a dose-dependent manner. In further results, AKR1C3 expression was decreased in both the xenograft tumor tissues and the CRPC cell lines following genistein gavage feeding compared to the control group, with the reduction becoming more obvious as the concentration of genistein was increased. When the genistein was combined with AKR1C3 small interfering ribonucleic acid and an AKR1C3 inhibitor (ASP-9521), the inhibitory effect on the AKR1C3 was more pronounced. In addition, the molecular docking results suggested that the genistein had a strong affinity with the AKR1C3, and that it could be a promising AKR1C3 inhibitor. Conclusion: Genistein inhibits the progression of CRPC via the suppression of AKR1C3.

Indexed as

AKR1C3castration-resistant prostate cancergenisteinPhytochemicalsprostate cancer

Identifiers

PMID36794010
PMCPMC9899042
OpenAlexW4319795342

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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.