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Apobec-1 complementation factor regulates cell migration and apoptosis through Dickkopf1 by acting on its 3' untranslated region in MCF7 cells.

Abstract A1CF (apobec-1 complementation factor) acts as a component of the apolipoprotein-B messenger RNA editing complex. Previous researches mainly focused on its post-transcriptional cytidine to uridine RNA editing. However, few study reported its role in progression of breast carcinoma cells. Wound healing assay and flow cytometry were applied to detect the migration and apoptosis; western blot, real-time polymerase chain reaction, and dual-luciferase assays were applied to investigate the potential regulation mechanism of A1CF-mediated cell migration and apoptosis. Knockdown of A1CF decreased cell migration and enhanced cell apoptosis in MCF7 cells in vitro. Western blot analysis showed that knockdown of A1CF decreased Dickkopf1 but increased c-Myc and β-catenin expression, and overexpression of A1CF can get opposite results. Knockdown of Dickkopf1 in A1CF-overexpressed cells decreased cell migration and enhanced cell apoptosis compared with A1CF-overexpressed cells. Luciferase-fused 3' untranslated region of human Dickkopf1 activity was highly upregulated in A1CF-overexpressed MCF7 cells, but this upregulation can be inhibited by mutating conserved binding motifs of Dickkopf1 3' untranslated region. A1CF played a crucial role in cell migration and survival through affecting 3' untranslated region of Dickkopf1 to upregulate its expression in MCF7 cells.
PMID
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Authors

Mayor MeshTerms
Keywords

Apobec-1 complementation factor

Dickkopf1

MCF7 cells

apoptosis

migration

Journal Title tumour biology : the journal of the international society for oncodevelopmental biology and medicine
Publication Year Start




PMID- 28639893
OWN - NLM
STAT- MEDLINE
DA  - 20170622
DCOM- 20170711
LR  - 20170713
IS  - 1423-0380 (Electronic)
IS  - 1010-4283 (Linking)
VI  - 39
IP  - 6
DP  - 2017 Jun
TI  - Apobec-1 complementation factor regulates cell migration and apoptosis through
      Dickkopf1 by acting on its 3' untranslated region in MCF7 cells.
PG  - 1010428317706218
LID - 10.1177/1010428317706218 [doi]
AB  - A1CF (apobec-1 complementation factor) acts as a component of the
      apolipoprotein-B messenger RNA editing complex. Previous researches mainly
      focused on its post-transcriptional cytidine to uridine RNA editing. However, few
      study reported its role in progression of breast carcinoma cells. Wound healing
      assay and flow cytometry were applied to detect the migration and apoptosis;
      western blot, real-time polymerase chain reaction, and dual-luciferase assays
      were applied to investigate the potential regulation mechanism of A1CF-mediated
      cell migration and apoptosis. Knockdown of A1CF decreased cell migration and
      enhanced cell apoptosis in MCF7 cells in vitro. Western blot analysis showed that
      knockdown of A1CF decreased Dickkopf1 but increased c-Myc and beta-catenin
      expression, and overexpression of A1CF can get opposite results. Knockdown of
      Dickkopf1 in A1CF-overexpressed cells decreased cell migration and enhanced cell 
      apoptosis compared with A1CF-overexpressed cells. Luciferase-fused 3'
      untranslated region of human Dickkopf1 activity was highly upregulated in
      A1CF-overexpressed MCF7 cells, but this upregulation can be inhibited by mutating
      conserved binding motifs of Dickkopf1 3' untranslated region. A1CF played a
      crucial role in cell migration and survival through affecting 3' untranslated
      region of Dickkopf1 to upregulate its expression in MCF7 cells.
FAU - Yan, Xin
AU  - Yan X
AD  - 1 The College of Laboratory Medicine, Chongqing Medical University, Chongqing,
      China.
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Li, Qianyin
AU  - Li Q
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Ni, Dongsheng
AU  - Ni D
AD  - 1 The College of Laboratory Medicine, Chongqing Medical University, Chongqing,
      China.
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Xie, Yajun
AU  - Xie Y
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - He, Qingling
AU  - He Q
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Wan, Qianya
AU  - Wan Q
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Liu, Yamin
AU  - Liu Y
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Lyu, Zhongshi
AU  - Lyu Z
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Mao, Zhaomin
AU  - Mao Z
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
FAU - Zhou, Qin
AU  - Zhou Q
AD  - 2 Division of Molecular Nephrology and the Creative Training Center for
      Undergraduates, The Ministry of Education Key Laboratory of Laboratory Medical
      Diagnostics, The College of Laboratory Medicine, Chongqing Medical University,
      Chongqing, China.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Tumour Biol
JT  - Tumour biology : the journal of the International Society for Oncodevelopmental
      Biology and Medicine
JID - 8409922
RN  - 0 (3' Untranslated Regions)
RN  - 0 (DKK1 protein, human)
RN  - 0 (Intercellular Signaling Peptides and Proteins)
RN  - 0 (RNA-Binding Proteins)
RN  - 0 (beta Catenin)
RN  - EC 3.5.4.36 (APOBEC-1 Deaminase)
RN  - EC 3.5.4.36 (APOBEC1 protein, human)
SB  - IM
MH  - 3' Untranslated Regions
MH  - APOBEC-1 Deaminase/*genetics
MH  - Apoptosis/genetics
MH  - Breast Neoplasms/*genetics/pathology
MH  - Cell Movement/genetics
MH  - Female
MH  - Gene Expression Regulation, Neoplastic
MH  - Gene Knockdown Techniques
MH  - Humans
MH  - Intercellular Signaling Peptides and Proteins/biosynthesis/*genetics
MH  - MCF-7 Cells
MH  - Protein Binding
MH  - RNA Editing/genetics
MH  - RNA-Binding Proteins/*genetics
MH  - beta Catenin/genetics
OTO - NOTNLM
OT  - Apobec-1 complementation factor
OT  - Dickkopf1
OT  - MCF7 cells
OT  - apoptosis
OT  - migration
EDAT- 2017/06/24 06:00
MHDA- 2017/07/14 06:00
CRDT- 2017/06/23 06:00
AID - 10.1177/1010428317706218 [doi]
PST - ppublish
SO  - Tumour Biol. 2017 Jun;39(6):1010428317706218. doi: 10.1177/1010428317706218.