PMID- 31542393
OWN - NLM
STAT- MEDLINE
DCOM- 20200402
LR  - 20200402
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 189
IP  - 12
DP  - 2019 Dec
TI  - Wasf3 Deficiency Reveals Involvement in Metastasis in a Mouse Model of Breast 
      Cancer.
PG  - 2450-2458
LID - S0002-9440(19)30716-3 [pii]
LID - 10.1016/j.ajpath.2019.08.012 [doi]
AB  - The WASF3 gene has been implicated in cancer cell movement, invasion, and 
      metastasis by regulating genetic pathways important in these processes. Invasion 
      and metastasis assays, however, are largely centered on xenograft models in 
      immune-compromised mice. To facilitate analysis of the role of WASF3 in the 
      spontaneous development of cancer cell metastasis, we generated a Wasf3 null 
      strain by deleting exons 4 and 5, which encode essential motifs for Wasf3 
      function. On exposure to cre-recombinase a stop codon is generated immediately 
      downstream in exon 6. Using a cytomegalovirus (CMV)-cre strain, Wasf3 
      constitutively was inactivated, which led to viable mice with no visible 
      morphologic or behavioral abnormalities. There was no abnormal development or 
      function of the mouse mammary gland in the Wasf3 null mice and brain development 
      was normal. In the mouse mammary tumor virus (MMTV)-driven polyoma middle-T 
      oncogene strain, which shows early onset breast cancer development and 
      metastasis, Wiskott-Aldrich syndrome protein family member 3 (Wasf3) is 
      up-regulated in metastatic lesions. When this oncogene was introduced onto the 
      Wasf3-null background, although metastasis was observed in these mice, there was 
      a reduction in the number and size of metastatic lesions in the lungs. These data 
      provide evidence for a role in WASF3 in the development of metastasis in a 
      spontaneous model of breast cancer.
CI  - Copyright (c) 2019 American Society for Investigative Pathology. Published by 
      Elsevier Inc. All rights reserved.
FAU - Qin, Haiyan
AU  - Qin H
AD  - Georgia Cancer Center, Augusta University, Augusta, Georgia.
FAU - Lu, Sumin
AU  - Lu S
AD  - Georgia Cancer Center, Augusta University, Augusta, Georgia.
FAU - Thangaraju, Muthusamy
AU  - Thangaraju M
AD  - Department of Biochemistry and Molecular Biology, Augusta University, Augusta, 
      Georgia.
FAU - Cowell, John K
AU  - Cowell JK
AD  - Georgia Cancer Center, Augusta University, Augusta, Georgia. Electronic address: 
      jcowell@augusta.edu.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190919
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (WASF3 protein, human)
RN  - 0 (Wasf3 protein, mouse)
RN  - 0 (Wiskott-Aldrich Syndrome Protein Family)
SB  - IM
MH  - Animals
MH  - Breast Neoplasms/genetics/metabolism/*pathology
MH  - Cell Movement
MH  - Cohort Studies
MH  - Disease Models, Animal
MH  - Female
MH  - *Gene Expression Regulation, Neoplastic
MH  - Humans
MH  - Lung Neoplasms/genetics/metabolism/*secondary
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Neoplasm Invasiveness
MH  - Signal Transduction
MH  - Tumor Cells, Cultured
MH  - Wiskott-Aldrich Syndrome Protein Family/genetics/*metabolism
EDAT- 2019/09/23 06:00
MHDA- 2020/04/03 06:00
CRDT- 2019/09/23 06:00
PHST- 2019/03/14 00:00 [received]
PHST- 2019/08/08 00:00 [revised]
PHST- 2019/08/13 00:00 [accepted]
PHST- 2019/09/23 06:00 [pubmed]
PHST- 2020/04/03 06:00 [medline]
PHST- 2019/09/23 06:00 [entrez]
AID - S0002-9440(19)30716-3 [pii]
AID - 10.1016/j.ajpath.2019.08.012 [doi]
PST - ppublish
SO  - Am J Pathol. 2019 Dec;189(12):2450-2458. doi: 10.1016/j.ajpath.2019.08.012. Epub 
      2019 Sep 19.