A novel program of infiltrative control in astrocytomas: ADAM23 depletion promotes cell invasion by activating <bold>γ</bold>-secretase complex

Imagem de Miniatura
Arquivos
art_JANDREY_A_novel_program_of_infiltrative_control_in_astrocytomas_2023.PDF (1.29 MB)
Citações na Scopus
0
Tipo de produção
article
Data de publicação
2023
DOI
Scopus
Web of Science
PubMed
Título da Revista
ISSN da Revista
Título do Volume
Editora
OXFORD UNIV PRESS
Autores
JANDREY, Elisa Helena Farias
BARNABE, Gabriela Filoso
MALDAUN, Marcos
ASPRINO, Paula Fontes
SANTOS, Natalia Cristina dos
INOUE, Lilian Tiemi
ROZANSKI, Andrei
GALANTE, Pedro Alexandre Favoretto
Citação
NEURO-ONCOLOGY ADVANCES, v.5, n.1, article ID vdad147, 13p, 2023
Projetos de Pesquisa
Unidades Organizacionais
Fascículo
Resumo
Background. Infiltration is a life-threatening growth pattern in malignant astrocytomas and a significant cause of therapy resistance. It results in the tumor cell spreading deeply into the surrounding brain tissue, fostering tumor recurrence and making complete surgical resection impossible. We need to thoroughly understand the mechanisms underlying diffuse infiltration to develop effective therapies.Methods We integrated in vitro and in vivo functional assays, RNA sequencing, clinical, and expression information from public data sets to investigate the role of ADAM23 expression coupling astrocytoma's growth and motility.Results. ADAM23 downregulation resulted in increased infiltration, reduced tumor growth, and improved overall survival in astrocytomas. Additionally, we show that ADAM23 deficiency induces gamma-secretase (GS) complex activity, contributing to the production and deposition of the Amyloid-beta and release of NICD. Finally, GS ablation in ADAM23-low astrocytomas induced a significant inhibitory effect on the invasive programs.Conclusions. Our findings reveal a role for ADAM23 in regulating the balance between cell proliferation and invasiveness in astrocytoma cells, proposing GS inhibition as a therapeutic option in ADAM23 low-expressing astrocytomas.
Palavras-chave
ADAM family, astrocytoma, Invasion, signal transduction, gamma-secretase
URI
https://observatorio.fm.usp.br/handle/OPI/57974
Referências
  1. Benitez JA, 2018, JOVE-J VIS EXP, DOI 10.3791/57448
  2. Blalock EM, 2004, P NATL ACAD SCI USA, V101, P2173, DOI 10.1073/pnas.0308512100
  3. Borgonovo ZLM, 2018, NEUROSCIENCE, V384, P165, DOI 10.1016/j.neuroscience.2018.05.016
  4. Calmon MF, 2007, CANCER GENET CYTOGEN, V173, P31, DOI 10.1016/j.cancergencyto.2006.09.008
  5. Chen AC, 2015, J CELL BIOL, V211, P1157, DOI 10.1083/jcb.201502001
  6. Choi JS, 2009, INT J CANCER, V124, P1258, DOI 10.1002/ijc.24023
  7. Chokshi CR, 2021, NEURO-ONCOLOGY, V23, P175
  8. Costa ET, 2015, ONCOGENE, V34, P1270, DOI 10.1038/onc.2014.70
  9. Costa ET., 2018, Proteases and Cancer. Methods in Molecular Biology, P1731
  10. Costa FF, 2004, ONCOGENE, V23, P1481, DOI 10.1038/sj.onc.1207263
  11. Darmanis S, 2017, CELL REP, V21, P1399, DOI 10.1016/j.celrep.2017.10.030
  12. Dohda T, 2007, EXP CELL RES, V313, P3141, DOI 10.1016/j.yexcr.2007.04.027
  13. Ehehalt R, 2003, J CELL BIOL, V160, P113, DOI 10.1083/jcb.200207113
  14. Fedorov A, 2012, MAGN RESON IMAGING, V30, P1323, DOI 10.1016/j.mri.2012.05.001
  15. Furnari FB, 2007, GENE DEV, V21, P2683, DOI 10.1101/gad.1596707
  16. Ghanbari-Movahed M, 2021, MOLECULES, V26, DOI 10.3390/molecules26040972
  17. Conceiçao ALG, 2015, J CANCER, V6, P593, DOI 10.7150/jca.11238
  18. Haapasalo A, 2011, J ALZHEIMERS DIS, V25, P3, DOI 10.3233/JAD-2011-101065
  19. Hovinga KE, 2010, STEM CELLS, V28, P1019, DOI 10.1002/stem.429
  20. Hsia HE, 2019, CELL MOL LIFE SCI, V76, P3055, DOI 10.1007/s00018-019-03173-7
  21. Hu CY, 2011, INT J EXP PATHOL, V92, P333, DOI 10.1111/j.1365-2613.2011.00766.x
  22. Krusche B, 2016, ELIFE, V5, DOI 10.7554/eLife.14845
  23. Kwon NS, 2017, ONCOTARGETS THER, V10, P2721, DOI 10.2147/OTT.S138912
  24. Liau BB, 2017, CELL STEM CELL, V20, P233, DOI 10.1016/j.stem.2016.11.003
  25. Louis DN, 2021, NEURO-ONCOLOGY, V23, P1231, DOI 10.1093/neuonc/noab106
  26. Ma RQ, 2018, PATHOL RES PRACT, V214, P1115, DOI 10.1016/j.prp.2018.06.007
  27. Magold AI, 2009, PLOS ONE, V4, DOI 10.1371/journal.pone.0006952
  28. Markus-Koch A, 2017, CELL MOL BIOL LETT, V22, DOI 10.1186/s11658-017-0045-1
  29. Matsumura N, 2014, J BIOL CHEM, V289, P5109, DOI 10.1074/jbc.M113.510131
  30. McCaw TR, 2021, ONCOLOGIST, V26, pE608, DOI 10.1002/onco.13627
  31. Nakada M, 2010, INT J CANCER, V126, P1155, DOI 10.1002/ijc.24849
  32. Nasrolahi A, 2023, CELL SIGNAL, V101, DOI 10.1016/j.cellsig.2022.110493
  33. Ozawa Tomoko, 2010, J Vis Exp, DOI 10.3791/1986
  34. Pang L, 2019, CANCERS, V11, DOI 10.3390/cancers11122025
  35. Saito N, 2014, STEM CELLS, V32, P301, DOI 10.1002/stem.1528
  36. Schroeter EH, 1998, NATURE, V393, P382, DOI 10.1038/30756
  37. SILBERGELD DL, 1991, J NEURO-ONCOL, V10, P179, DOI 10.1007/BF00146880
  38. Thal DR, 2008, J CELL MOL MED, V12, P1848, DOI 10.1111/j.1582-4934.2008.00411.x
  39. Torre IG, 2020, SOFTWAREX, V12, DOI 10.1016/j.softx.2020.100574
  40. Verbisck NV, 2009, CANCER RES, V69, P5546, DOI 10.1158/0008-5472.CAN-08-2976
  41. Viswanathan R, 2021, EMBO J, V40, DOI 10.15252/embj.2020107245
  42. Vollmann-Zwerenz A, 2020, INT J MOL SCI, V21, DOI 10.3390/ijms21061932
  43. Wang YM, 2012, CELL BIOL INT, V36, P1275, DOI 10.1042/CBI20120154
  44. Wolfe MS, 2019, BIOCHEMISTRY-US, V58, P2953, DOI 10.1021/acs.biochem.9b00401
  45. Xu R, 2016, CLIN CANCER RES, V22, P4786, DOI 10.1158/1078-0432.CCR-16-0048

Coleções
Artigos e Materiais de Revistas Científicas - FM/MNE
Artigos e Materiais de Revistas Científicas - FM/MDR
Artigos e Materiais de Revistas Científicas - LIM/05
Artigos e Materiais de Revistas Científicas - LIM/15
Artigos e Materiais de Revistas Científicas - LIM/24