Evidence map›Paper›PMID 27203547›Full record

ArticleOncotarget2016

Functional role and tobacco smoking effects on methylation of CYP1A1 gene in prostate cancer.

Yozo Mitsui, Inik Chang, Taku Kato, Yutaka Hashimoto, Soichiro Yamamura, Shinichiro Fukuhara, Darryn K Wong, Marisa Shiina, Mitsuho Imai-Sumida, Shahana Majid and 6 more

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2016. 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, 27 citations in OpenAlex.

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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

16 authors at 5 institutions in 3 countries.

Yozo MitsuiDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Inik ChangDepartment of Oral Biology, Yonsei University College of Density, Seoul, 120-752, South Korea.
Taku KatoDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Yutaka HashimotoDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Soichiro YamamuraDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Shinichiro FukuharaDepartment of Urology, Osaka University Graduate School of Medicine, Suita, 565-0871, Japan.
Darryn K WongDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Marisa ShiinaDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Mitsuho Imai-SumidaDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Shahana MajidDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Sharanjot SainiDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Hiroaki ShiinaDepartment of Urology, Shimane University Faculty of Medicine, Izumo, 693-8501, Japan.
Koichi NakajimaDepartment of Urology, Toho University Faculty of Medicine, Tokyo, 143-8540, Japan.
Guoren DengDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Rajvir DahiyaDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
Yuichiro TanakaDepartment of Surgery/Urology, Veterans Affairs Health Care System, San Francisco, California 94121, USA.
University of California, San Francisco · USOsaka University · JPShimane University · JPToho University · JPYonsei University · KR

Funding

MicroRNAs in the Progression and Metastisis of Prostate CancerR01CA138642 · NCI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI DAHIYA, RAJVIR · 2010 to 2014
$2.6M
Chemo-dietary prevention, miRNAs, epigenetic and prostate cancerR01CA160079 · NCI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI DAHIYA, RAJVIR · 2011 to 2015
$2.2M
Genetic factors for race related prostate cancer.U01CA184966 · NCI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI DAHIYA, RAJVIR · 2015 to 2019
$1.6M
Racial differences in CYP1B1 polymorphisms and risks for prostate cancerR21CA185003 · NCI · NORTHERN CALIFORNIA INSTITUTE/RES/EDU · PI TANAKA, YUICHIRO · 2015 to 2016
$367k
BLRD VA I01 BX000726NCI NIH HHS R01 CA138642NCI NIH HHS R01 CA160079NCI NIH HHS R21 CA185003NCI NIH HHS U01 CA184966
6 · The paper itself

Abstract

Cytochrome P450 (CYP) 1A1 is a phase I enzyme that can activate various compounds into reactive forms and thus, may contribute to carcinogenesis. In this study, we investigated the expression, methylation status, and functional role of CYP1A1 on prostate cancer cells. Increased expression of CYP1A1 was observed in all cancer lines (PC-3, LNCaP, and DU145) compared to BPH-1 (P < 0.05); and was enhanced further by 5-aza-2'-deoxycytidine treatment (P < 0.01). Methylation-specific PCR (MSP) and sequencing of bisulfite-modified DNA of the xenobiotic response element (XRE) enhancer site XRE-1383 indicated promoter methylation as a regulator of CYP1A1 expression. In tissue, microarrays showed higher immunostaining of CYP1A1 in prostate cancer than normal and benign prostatic hyperplasia (BPH; P < 0.001), and methylation analyses in clinical specimens revealed significantly lower methylation levels in cancer compared to BPH at all enhancer sites analyzed (XRE-1383, XRE-983, XRE-895; P < 0.01). Interestingly, smoking affected the XRE-1383 site where the methylation level was much lower in cancer tissues from smokers than non-smokers (P < 0.05). CYP1A1 levels are thus increased in prostate cancer and to determine the functional effect of CYP1A1 on cells, we depleted the gene in LNCaP and DU145 by siRNA. We observe that CYP1A1 knockdown decreased cell proliferation (P < 0.05) and increased apoptosis (P < 0.01) in both cell lines. We analyzed genes affected by CYP1A1 silencing and found that apoptosis-related BCL2 was significantly down-regulated. This study supports an oncogenic role for CYP1A1 in prostate cancer via promoter hypomethylation that is influenced by tobacco smoking, indicating CYP1A1 to be a promising target for prostate cancer treatment.

Indexed as

DNA MethylationAgedAged, 80 and overApoptosisAzacitidineCell Line, TumorCpG IslandsCytochrome P-450 CYP1A1DecitabineEnhancer Elements, GeneticEpigenesis, GeneticGene Expression ProfilingGene Expression Regulation, NeoplasticHumansMaleMiddle AgedAzacitidineCYP1A1 protein, humanCytochrome P-450 CYP1A1Decitabinehydrogen sulfiteSulfitesXenobioticscytochrome P450 1A1methylationprostate cancertobacco smoking

Identifiers

PMID27203547
PMCPMC5226494
OpenAlexW2395308074

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.