Truncated WT1 Protein Isoform Expression Is Increased in MCF-7 Cells with Long-Term Estrogen Depletion.
Journal
International journal of breast cancer
ISSN: 2090-3170
Titre abrégé: Int J Breast Cancer
Pays: Egypt
ID NLM: 101568103
Informations de publication
Date de publication:
2021
2021
Historique:
received:
12
05
2020
revised:
26
05
2021
accepted:
27
09
2021
entrez:
30
11
2021
pubmed:
1
12
2021
medline:
1
12
2021
Statut:
epublish
Résumé
The Initially, the expression of 52-54 kDa protein isoform of WT1 in the breast cancer cell line ER (+) was detected by western blot and was absent in ER (-), and the 36-38 kDa protein isoform of WT1 was detected in all cell lines analyzed. The analysis of alternative splicing by RT-PCR shows that the 17AA (+)/KTS (-) isoform of WT1 was the most frequent in the four cell lines analyzed. Modulation of protein isoforms showed differential expression of WT1 isoforms dependent on estrogen receptor. The absence of 52-54 kDa and the presence of the 36-38 kDa protein isoform of WT1 were detected in ER-negative breast cancer cell lines classified as advanced stage cells. Long-term estrogen depletion assay in MCF-7 cells increased the expression of the 36-38 kDa isoform and reduced the 52-54 kDa isoform, and these cells show an increase in the expression of tumor markers of ER and Her2/neu. MCF-7 LTED cells showed low proliferation and insensitivity to tamoxifen compared to MCF-7 cells in normal conditions. These results support the theory about the relationship of the 36-38 kDa isoform of WT1 and the absence of ER function in advanced breast cancer.
Sections du résumé
BACKGROUND
BACKGROUND
The
RESULTS
RESULTS
Initially, the expression of 52-54 kDa protein isoform of WT1 in the breast cancer cell line ER (+) was detected by western blot and was absent in ER (-), and the 36-38 kDa protein isoform of WT1 was detected in all cell lines analyzed. The analysis of alternative splicing by RT-PCR shows that the 17AA (+)/KTS (-) isoform of WT1 was the most frequent in the four cell lines analyzed.
CONCLUSIONS
CONCLUSIONS
Modulation of protein isoforms showed differential expression of WT1 isoforms dependent on estrogen receptor. The absence of 52-54 kDa and the presence of the 36-38 kDa protein isoform of WT1 were detected in ER-negative breast cancer cell lines classified as advanced stage cells. Long-term estrogen depletion assay in MCF-7 cells increased the expression of the 36-38 kDa isoform and reduced the 52-54 kDa isoform, and these cells show an increase in the expression of tumor markers of ER and Her2/neu. MCF-7 LTED cells showed low proliferation and insensitivity to tamoxifen compared to MCF-7 cells in normal conditions. These results support the theory about the relationship of the 36-38 kDa isoform of WT1 and the absence of ER function in advanced breast cancer.
Identifiants
pubmed: 34845427
doi: 10.1155/2021/6282514
pmc: PMC8627338
doi:
Types de publication
Journal Article
Langues
eng
Pagination
6282514Informations de copyright
Copyright © 2021 Saavedra-Alonso Santiago et al.
Déclaration de conflit d'intérêts
The authors declare that they have no conflicts of interest.
Références
Proc Natl Acad Sci U S A. 1997 Jul 22;94(15):8132-7
pubmed: 9223327
Asian Pac J Cancer Prev. 2016;17(S3):43-6
pubmed: 27165206
J Biol Chem. 2006 Sep 22;281(38):28122-30
pubmed: 16698800
Appl Immunohistochem Mol Morphol. 2005 Jun;13(2):132-7
pubmed: 15894924
J Biol Chem. 1995 May 5;270(18):10878-84
pubmed: 7738027
Ann Hematol. 2004 Dec;83(12):745-50
pubmed: 15340762
Int J Cancer. 2002 Jul 20;100(3):297-303
pubmed: 12115544
Proc Natl Acad Sci U S A. 1991 Nov 1;88(21):9618-22
pubmed: 1658787
Cancer Sci. 2003 Aug;94(8):712-7
pubmed: 12901797
Cancer Sci. 2003 Jun;94(6):523-9
pubmed: 12824878
Nat Genet. 1996 Mar;12(3):329-31
pubmed: 8589729
J Biol Chem. 1996 Apr 12;271(15):8646-54
pubmed: 8621495
Am J Pathol. 2017 Oct;187(10):2152-2162
pubmed: 28733194
Science. 1990 Nov 30;250(4985):1259-62
pubmed: 2244209
Clin Cancer Res. 2002 May;8(5):1167-71
pubmed: 12006533
Tumori. 2013 Nov-Dec;99(6):715-22
pubmed: 24503796
Proc Natl Acad Sci U S A. 1993 Jun 1;90(11):5100-4
pubmed: 8389468
Oncogene. 2005 Feb 24;24(9):1648-52
pubmed: 15674342
Anticancer Res. 2014 Mar;34(3):1333-42
pubmed: 24596380
Blood. 1998 Apr 15;91(8):2969-76
pubmed: 9531608
Oncogene. 2007 May 17;26(23):3423-30
pubmed: 17160023
Jpn J Clin Oncol. 2004 Feb;34(2):74-7
pubmed: 15067099
J Biol Chem. 2003 May 30;278(22):19995-20005
pubmed: 12644474
Leuk Res. 1999 May;23(5):499-505
pubmed: 10374864
Hum Mol Genet. 2004 Feb 15;13(4):405-15
pubmed: 14681303
Genes Dev. 2001 Feb 1;15(3):328-39
pubmed: 11159913
PLoS One. 2015 Jun 19;10(6):e0130578
pubmed: 26090994
J Biol Chem. 2011 Dec 23;286(51):43634-43643
pubmed: 22030397
J Biol Chem. 2012 Sep 21;287(39):32875-80
pubmed: 22898820
Proc Natl Acad Sci U S A. 1995 Nov 21;92(24):11105-9
pubmed: 7479946
Biochem Biophys Res Commun. 2002 Jul 26;295(4):784-90
pubmed: 12127961
Mol Diagn. 2000 Jun;5(2):117-28
pubmed: 11066013
Cancer Sci. 2006 Apr;97(4):259-70
pubmed: 16630117
Mol Cell Biol. 1995 Mar;15(3):1489-98
pubmed: 7862142
Jpn J Cancer Res. 1999 Feb;90(2):194-204
pubmed: 10189890
Cancer Sci. 2003 Mar;94(3):271-6
pubmed: 12824921
Am J Cancer Res. 2015 Sep 15;5(10):2929-43
pubmed: 26693050
Cancer Sci. 2004 Jul;95(7):583-7
pubmed: 15245594
Oncol Rep. 2010 Apr;23(4):1109-17
pubmed: 20204298
Cancer Res. 2001 Feb 1;61(3):921-5
pubmed: 11221883
Nucleic Acids Res. 1998 Apr 1;26(7):1784-92
pubmed: 9512553
Oncogene. 2006 Jul 13;25(30):4217-29
pubmed: 16518414
Anticancer Res. 2013 Aug;33(8):3335-40
pubmed: 23898100
Leukemia. 2007 May;21(5):868-76
pubmed: 17361230
Breast Cancer Res Treat. 2003 Sep;81(1):81-93
pubmed: 14531500
Oncogene. 2004 Sep 9;23(41):6933-41
pubmed: 15286719
PLoS One. 2013 Aug 01;8(8):e68837
pubmed: 23936312
Int J Oncol. 2008 Mar;32(3):701-11
pubmed: 18292948
J Biol Chem. 1999 Aug 13;274(33):23456-62
pubmed: 10438524
Eur J Histochem. 2015 Jun 29;59(2):2499
pubmed: 26150159
Blood. 2006 Jun 15;107(12):4695-702
pubmed: 16484585
EMBO J. 1999 Jul 15;18(14):3990-4003
pubmed: 10406804
Clin Cancer Res. 2006 Jan 1;12(1):34-42
pubmed: 16397021
Sci Rep. 2017 Mar 27;7:45255
pubmed: 28345629
Methods. 2001 Dec;25(4):402-8
pubmed: 11846609