Evidence map›Paper›PMID 26626260›Full record

ArticleBMC cancer2015

CYP1B1 promotes tumorigenesis via altered expression of CDC20 and DAPK1 genes in renal cell carcinoma.

Yozo Mitsui, Inik Chang, Shinichiro Fukuhara, Miho Hiraki, Naoko Arichi, Hiroaki Yasumoto, Hiroshi Hirata, Soichiro Yamamura, Varahram Shahryari, Guoren Deng and 5 more

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in BMC cancer, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

26 citing papers in PubMed, 54 citations in OpenAlex.

  1. Trial
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  7. Frontiers in pharmacology · 2024
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  8. Review
  9. Saudi medical journal · 2023
    Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Cytochrome P450 Enzymes and Drug Metabolism in Humans.International journal of molecular sciences · 2021
    Review
  15. Article
  16. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors at 5 institutions in 3 countries.

Yozo MitsuiDepartment of Urology Shimane University Faculty of Medicine, 89-1 Enya-cho, 693-8501, Izumo, Japan. mitsui@med.shimane-u.ac.jp.
Inik ChangDepartment of Oral Biology, Yonsei University College of Density, Seoul, South Korea. ichang@yuhs.ac.
Shinichiro FukuharaDepartment of Urology, Osaka University Graduate School of Medicine, 565-0871, Suita, Japan. fukuharajua@gmail.com.
Miho HirakiDepartment of Urology Shimane University Faculty of Medicine, 89-1 Enya-cho, 693-8501, Izumo, Japan. mhiraki@med.shimane-u.ac.jp.
Naoko ArichiDepartment of Urology Shimane University Faculty of Medicine, 89-1 Enya-cho, 693-8501, Izumo, Japan. naoko-a@med.shimane-u.ac.jp.
Hiroaki YasumotoDepartment of Urology Shimane University Faculty of Medicine, 89-1 Enya-cho, 693-8501, Izumo, Japan. hiyasumo@med.shimane-u.ac.jp.
Hiroshi HirataDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. hiroucsf@gmail.com.
Soichiro YamamuraDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. socihiro.yamamura@va.gov.
Varahram ShahryariDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. varahram.shahryari@ncire.org.
Guoren DengDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. guoren.deng@ucsf.edu.
Darryn K WongDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. darrynwong@ucla.edu.
Shahana MajidDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. shankhan999@yahoo.com.
Hiroaki ShiinaDepartment of Urology Shimane University Faculty of Medicine, 89-1 Enya-cho, 693-8501, Izumo, Japan. hshiina@med.shimane-u.ac.jp.
Rajvir DahiyaDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. rdahiya@gmail.com.
Yuichiro TanakaDepartment of Urology, San Francisco Veterans Affairs Medical Center and University of California San Francisco, Bldg 42 Rm 109, San Francisco, CA, 94121, USA. Yuichiro.tanaka@ucsf.edu.
Shimane University · JPUniversity of California, San Francisco · USSan Francisco VA Medical Center · USOsaka University · JPYonsei University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCytochrome P450 1B1 (CYP1B1) has been shown to be up-regulated in many types of cancer including renal cell carcinoma (RCC). Several reports have shown that CYP1B1 can influence the regulation of tumor development; however, its role in RCC has not been well investigated. The aim of the present study was to determine the functional effects of CYP1B1 gene on tumorigenesis in RCC.

methodsExpression of CYP1B1 was determined in RCC cell lines, and tissue microarrays of 96 RCC and 25 normal tissues. To determine the biological significance of CYP1B1 in RCC progression, we silenced the gene in Caki-1 and 769-P cells by RNA interference and performed various functional analyses.

resultsFirst, we confirmed that CYP1B1 protein expression was significantly higher in RCC cell lines compared to normal kidney tissue. This trend was also observed in RCC samples (p < 0.01). Interestingly, CYP1B1 expression was associated with tumor grade and stage. Next, we silenced the gene in Caki-1 and 769-P cells by RNA interference and performed various functional analyses to determine the biological significance of CYP1B1 in RCC progression. Inhibition of CYP1B1 expression resulted in decreased cell proliferation, migration and invasion of RCC cells. In addition, reduction of CYP1B1 induced cellular apoptosis in Caki-1. We also found that these anti-tumor effects on RCC cells caused by CYP1B1 depletion may be due to alteration of CDC20 and DAPK1 expression based on gene microarray and confirmed by real-time PCR. Interestingly, CYP1B1 expression was associated with CDC20 and DAPK1 expression in clinical samples.

conclusionsCYP1B1 may promote RCC development by inducing CDC20 expression and inhibiting apoptosis through the down-regulation of DAPK1. Our results demonstrate that CYP1B1 can be a potential tumor biomarker and a target for anticancer therapy in RCC.

Indexed as

ApoptosisCarcinoma, Renal CellCdc20 ProteinsCell Line, TumorCell MovementCytochrome P-450 CYP1B1Death-Associated Protein KinasesFemaleGene Expression Regulation, NeoplasticHumansKidney NeoplasmsMaleMiddle AgedNeoplasm InvasivenessUp-RegulationCDC20 protein, humanCdc20 ProteinsCYP1B1 protein, humanCytochrome P-450 CYP1B1DAPK1 protein, humanDeath-Associated Protein Kinases

Identifiers

PMID26626260
PMCPMC4665921
OpenAlexW2182824225

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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.