TY - JOUR
T1 - Cytotoxic effect caspase activation dependent of a genetically engineered fusion protein with a CD154 peptide mimetic (OmpC-CD154 p ) on B-NHL cell lines is mediated by the inhibition of bcl-6 and YY1 through MAPK p38 activation
AU - Pantoja-Escobar, Gerardo
AU - Morales-Martínez, Mario
AU - Vega, Gabriel G.
AU - Castro-Escarpulli, Graciela
AU - Vega, Mario I.
N1 - Publisher Copyright:
© 2018, © 2018 Informa UK Limited, trading as Taylor & Francis Group.
PY - 2019/3/21
Y1 - 2019/3/21
N2 - The interaction between CD40, and its ligand, CD154, is essential for the development of humoral and cellular immune responses. The selective inhibition or activation of this pathway forms the basis for the development of new therapeutics against immunologically based diseases and malignancies. We are developing a gene fusion of Salmonella typhi OmpC protein expressing the CD154 Tyr140-Ser-149 amino acid strand. This OmpC-CD154 binds CD40 and activates B cells. In this study, we demonstrate that OmpC-CD154 p treatment inhibits cell growth, proliferation and induced apoptosis in the B-NHL cell lines Raji and Ramos. The Bcl-2 family proteins were regulated and the Bcl-6 and YY1 oncoproteins were inhibited. p38 MAPK activation is an important mechanism underlying the effect on proliferation and apoptosis mediated by this fusion protein. This study establishes a basis for the possible use of fusion protein OmpC-CD154 as an alternative treatment for B-NHL.
AB - The interaction between CD40, and its ligand, CD154, is essential for the development of humoral and cellular immune responses. The selective inhibition or activation of this pathway forms the basis for the development of new therapeutics against immunologically based diseases and malignancies. We are developing a gene fusion of Salmonella typhi OmpC protein expressing the CD154 Tyr140-Ser-149 amino acid strand. This OmpC-CD154 binds CD40 and activates B cells. In this study, we demonstrate that OmpC-CD154 p treatment inhibits cell growth, proliferation and induced apoptosis in the B-NHL cell lines Raji and Ramos. The Bcl-2 family proteins were regulated and the Bcl-6 and YY1 oncoproteins were inhibited. p38 MAPK activation is an important mechanism underlying the effect on proliferation and apoptosis mediated by this fusion protein. This study establishes a basis for the possible use of fusion protein OmpC-CD154 as an alternative treatment for B-NHL.
KW - Bcl-6
KW - Non-Hodgkin lymphoma
KW - P38
KW - YY1
KW - apoptosis
KW - fusion protein
UR - http://www.scopus.com/inward/record.url?scp=85054347537&partnerID=8YFLogxK
U2 - 10.1080/10428194.2018.1516286
DO - 10.1080/10428194.2018.1516286
M3 - Artículo
C2 - 30277117
SN - 1042-8194
VL - 60
SP - 1062
EP - 1070
JO - Leukemia and Lymphoma
JF - Leukemia and Lymphoma
IS - 4
ER -