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Arsenic treatment increase Aurora-A overexpression through E2F1 activation in bladder cells.

Abstract Arsenic is a widely distributed metalloid compound that has biphasic effects on cultured cells. In large doses, arsenic can be toxic enough to trigger cell death. In smaller amounts, non-toxic doses may promote cell proliferation and induces carcinogenesis. Aberration of chromosome is frequently detected in epithelial cells and lymphocytes of individuals from arsenic contaminated areas. Overexpression of Aurora-A, a mitotic kinase, results in chromosomal instability and cell transformation. We have reported that low concentration (≦1 μM) of arsenic treatment increases Aurora-A expression in immortalized bladder urothelial E7 cells. However, how arsenic induces carcinogenesis through Aurora-A activation remaining unclear.
PMID
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Authors

Mayor MeshTerms
Keywords

Arsenic

Aurora-A

Bladder

Carcinogenesis

Journal Title bmc cancer
Publication Year Start




PMID- 28420331
OWN - NLM
STAT- MEDLINE
DA  - 20170419
DCOM- 20170425
LR  - 20170425
IS  - 1471-2407 (Electronic)
IS  - 1471-2407 (Linking)
VI  - 17
IP  - 1
DP  - 2017 Apr 18
TI  - Arsenic treatment increase Aurora-A overexpression through E2F1 activation in
      bladder cells.
PG  - 277
LID - 10.1186/s12885-017-3253-1 [doi]
AB  - BACKGROUND: Arsenic is a widely distributed metalloid compound that has biphasic 
      effects on cultured cells. In large doses, arsenic can be toxic enough to trigger
      cell death. In smaller amounts, non-toxic doses may promote cell proliferation
      and induces carcinogenesis. Aberration of chromosome is frequently detected in
      epithelial cells and lymphocytes of individuals from arsenic contaminated areas. 
      Overexpression of Aurora-A, a mitotic kinase, results in chromosomal instability 
      and cell transformation. We have reported that low concentration (<==1 muM) of
      arsenic treatment increases Aurora-A expression in immortalized bladder
      urothelial E7 cells. However, how arsenic induces carcinogenesis through Aurora-A
      activation remaining unclear. METHODS: Bromodeoxyuridine (BrdU) staining, MTT
      assay, and flow cytometry assay were conducted to determine cell proliferation.
      Messenger RNA and protein expression levels of Aurora-A were detected by reverse 
      transcriptional-PCR and Western blotting, respectively. Centrosome of cells was
      observed by immunofluorescent staining. The transcription factor of Aurora-A was 
      investigated by promoter activity, chromosome immunoprecipitation (ChIP), and
      small interfering RNA (shRNA) assays. Mouse model was utilized to confirm the
      relationship between arsenic and Aurora-A. RESULTS: We reveal that low dosage of 
      arsenic treatment increased cell proliferation is associated with accumulated
      cell population at S phase. We also detected increased Aurora-A expression at
      mRNA and protein levels in immortalized bladder urothelial E7 cells exposed to
      low doses of arsenic. Arsenic-treated cells displayed increased multiple
      centrosome which is resulted from overexpressed Aurora-A. Furthermore, the
      transcription factor, E2F1, is responsible for Aurora-A overexpression after
      arsenic treatment. We further disclosed that Aurora-A expression and cell
      proliferation were increased in bladder and uterus tissues of the BALB/c mice
      after long-term arsenic (1 mg/L) exposure for 2 months. CONCLUSION: We reveal
      that low dose of arsenic induced cell proliferation is through Aurora-A
      overexpression, which is transcriptionally regulated by E2F1 both in vitro and in
      vivo. Our findings disclose a new possibility that arsenic at low concentration
      activates Aurora-A to induce carcinogenesis.
FAU - Kao, Yu-Ting
AU  - Kao YT
AD  - Department of Microbiology and Immunology, College of Medicine, National Cheng
      Kung University, Tainan, Taiwan.
FAU - Wu, Chin-Han
AU  - Wu CH
AD  - Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung
      University, Tainan, Taiwan.
FAU - Wu, Shan-Ying
AU  - Wu SY
AD  - Department of Microbiology and Immunology, College of Medicine, National Cheng
      Kung University, Tainan, Taiwan.
FAU - Lan, Sheng-Hui
AU  - Lan SH
AD  - Department of Microbiology and Immunology, College of Medicine, National Cheng
      Kung University, Tainan, Taiwan.
FAU - Liu, Hsiao-Sheng
AU  - Liu HS
AD  - Department of Microbiology and Immunology, College of Medicine, National Cheng
      Kung University, Tainan, Taiwan. [email protected]
AD  - Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung
      University, Tainan, Taiwan. [email protected]
FAU - Tseng, Ya-Shih
AU  - Tseng YS
AD  - Department of Medical Laboratory Science and Biotechnology, College of Medicine
      and Life Science, Chung Hwa University of Medical technology, Tainan, Taiwan.
      [email protected]
LA  - eng
PT  - Journal Article
DEP - 20170418
PL  - England
TA  - BMC Cancer
JT  - BMC cancer
JID - 100967800
RN  - 0 (E2F1 Transcription Factor)
RN  - 0 (E2F1 protein, human)
RN  - EC 2.7.11.1 (Aurora Kinase A)
RN  - N712M78A8G (Arsenic)
SB  - IM
MH  - Animals
MH  - Arsenic/*toxicity
MH  - Aurora Kinase A/*biosynthesis
MH  - Blotting, Western
MH  - Carcinogenesis/drug effects
MH  - Carcinoma, Transitional Cell/*enzymology
MH  - Cell Line, Tumor
MH  - Cell Proliferation/drug effects
MH  - Chromatin Immunoprecipitation
MH  - E2F1 Transcription Factor/*metabolism
MH  - Flow Cytometry
MH  - Fluorescent Antibody Technique
MH  - Humans
MH  - Immunohistochemistry
MH  - Mice
MH  - Mice, Inbred BALB C
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Urinary Bladder Neoplasms/*enzymology
PMC - PMC5394624
OTO - NOTNLM
OT  - Arsenic
OT  - Aurora-A
OT  - Bladder
OT  - Carcinogenesis
EDAT- 2017/04/20 06:00
MHDA- 2017/04/26 06:00
CRDT- 2017/04/20 06:00
PHST- 2016/08/24 [received]
PHST- 2017/04/01 [accepted]
AID - 10.1186/s12885-017-3253-1 [doi]
AID - 10.1186/s12885-017-3253-1 [pii]
PST - epublish
SO  - BMC Cancer. 2017 Apr 18;17(1):277. doi: 10.1186/s12885-017-3253-1.

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