Academic Journal

Functional role and tobacco smoking effects on methylation ofCYP1A1gene in prostate cancer

Bibliographic Details
Title: Functional role and tobacco smoking effects on methylation ofCYP1A1gene in prostate cancer
Authors: Mitsui, Yozo, Chang, Inik, Kato, Taku, Hashimoto, Yutaka, Yamamura, Soichiro, Fukuhara, Shinichiro, Wong, Darryn K, Shiina, Marisa, Imai-Sumida, Mitsuho, Majid, Shahana, Saini, Sharanjot, Shiina, Hiroaki, Nakajima, Koichi, Deng, Guoren, Dahiya, Rajvir, Tanaka, Yuichiro
Contributors: College of Dentistry, Dept. of Oral Biology, Yozo Mitsui, Inik Chang, Taku Kato, Yutaka Hashimoto, Soichiro Yamamura, Shinichiro Fukuhara, Darryn K. Wong, Marisa Shiina, Mitsuho Imai-Sumida, Shahana Majid, Sharanjot Saini, Hiroaki Shiina, Koichi Nakajima, Guoren Deng, Rajvir Dahiya, Yuichiro Tanaka, Chang, In Ik
Source: Oncotarget
Oncotarget, vol 7, iss 31
Publisher Information: Impact Journals, LLC, 2016.
Publication Year: 2016
Subject Terms: Male, Aging, Prostatic Hyperplasia, Apoptosis, Polymerase Chain Reaction, Epigenesis, Genetic, 80 and over, 2.1 Biological and endogenous factors, Azacitidine/analogs & derivatives, Aetiology, Prostatic Neoplasms/metabolism, Promoter Regions, Genetic, Cancer, Oligonucleotide Array Sequence Analysis, Aged, 80 and over, DNA Methylation, Azacitidine/chemistry, Tumor, Prostatic Neoplasms/genetics, Prostate Cancer, Middle Aged, prostate cancer, 3. Good health, Gene Expression Regulation, Neoplastic, Enhancer Elements, Genetic, Azacitidine, Cytochrome P-450 CYP1A1/metabolism, cytochrome P450 1A1, Biotechnology, Research Paper, Urologic Diseases, Enhancer Elements, Oncology and Carcinogenesis, Decitabine, Cell Line, Xenobiotics, Promoter Regions, Genetic, Cell Line, Tumor, Tobacco, Genetics, Tobacco Smoking, Cytochrome P-450 CYP1A1, Sulfites, Humans, tobacco smoking, Aged, Neoplastic, Tobacco Smoke and Health, Cytochrome P-450 CYP1A1/genetics, Prevention, Gene Expression Profiling, Prostatic Hyperplasia/metabolism, Prostatic Neoplasms, Prostatic Hyperplasia/genetics, Gene Expression Regulation, Tissue Array Analysis, Tobacco Smoking/adverse effects, CpG Islands, methylation, Sulfites/chemistry, Xenobiotics/chemistry, Epigenesis
Description: 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.
Document Type: Article
Other literature type
File Description: application/pdf
Language: English
ISSN: 1949-2553
DOI: 10.18632/oncotarget.9470
Access URL: http://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=download&path%5B%5D=9470&path%5B%5D=29437
https://pubmed.ncbi.nlm.nih.gov/27203547
https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201902205667856850
https://escholarship.org/content/qt22s2h59f/qt22s2h59f.pdf?t=qanpgh
https://www.oncotarget.com/fulltext/9470
https://www.oncotarget.com/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=9470
http://www.impactjournals.com/oncotarget/index.php?journal=oncotarget&page=article&op=view&path%5B%5D=9470&path%5B%5D=0
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5226494/
https://escholarship.org/uc/item/22s2h59f
https://escholarship.org/content/qt22s2h59f/qt22s2h59f.pdf
Rights: CC BY
CC BY NC ND
Accession Number: edsair.doi.dedup.....cf5c5f3f4c15173f1324622c71d608c4
Database: OpenAIRE
Description
ISSN:19492553
DOI:10.18632/oncotarget.9470