TY - JOUR
T1 - The TGF-beta — smad pathway is inactivated in cronic lymphocytic leukemia cells
AU - Matveeva, A.
AU - Kovalevska, L.
AU - Kholodnyuk, I.
AU - Ivanivskaya, T.
AU - Kashuba, E.
N1 - Funding Information:
This work was supported by the Swedish Cancer Society, by matching grants from the Concern Foundation (Los Angeles, USA) and the Cancer Research Institute (New York, USA), and by the Academy of Science of Ukraine (grant No. 0112U002192).
Publisher Copyright:
Copyright © Experimental Oncology, 2017.
Copyright:
Copyright 2020 Elsevier B.V., All rights reserved.
PY - 2017/12
Y1 - 2017/12
N2 - Aim: To study the status of the tumor growth factor beta (TGFB) pathway in chronic lymphocytic leukemia (CLL) cells and to uncover molecular details underlying CLL cell genesis. ObjectsandMethods: The study was conducted on peripheral blood samples of patients with CLL using the following methods: RNA isolation, analysis of expression of transcription factors using RT2 profiler assay, bioinformatics analysis of publicly available data bases on expression. Results: We have shown that the TGFB — SMAD canonical pathway is not active in CLL cells. SMAD-responsive genes, such as BCL2L1 (BCL-XL), CCND2 (Cyclin D2), and MYC, are down-regulated in CLL cells compared with peripheral blood B cells of healthy donors. Conclusions: The TGFB-mediated signaling is not active in CLL cells due to low (or absent) expression of SMAD1, -4, -5, -9, and ATF-3. Expression and phosphorylation status of SMAD2 and -3 should be further elucidated in the future studies.
AB - Aim: To study the status of the tumor growth factor beta (TGFB) pathway in chronic lymphocytic leukemia (CLL) cells and to uncover molecular details underlying CLL cell genesis. ObjectsandMethods: The study was conducted on peripheral blood samples of patients with CLL using the following methods: RNA isolation, analysis of expression of transcription factors using RT2 profiler assay, bioinformatics analysis of publicly available data bases on expression. Results: We have shown that the TGFB — SMAD canonical pathway is not active in CLL cells. SMAD-responsive genes, such as BCL2L1 (BCL-XL), CCND2 (Cyclin D2), and MYC, are down-regulated in CLL cells compared with peripheral blood B cells of healthy donors. Conclusions: The TGFB-mediated signaling is not active in CLL cells due to low (or absent) expression of SMAD1, -4, -5, -9, and ATF-3. Expression and phosphorylation status of SMAD2 and -3 should be further elucidated in the future studies.
KW - B-cell chronic lymphocytic leukemia
KW - SMAD proteins
KW - TGFB — SMAD pathway
KW - Tumor growth factor beta
UR - http://www.scopus.com/inward/record.url?scp=85039958698&partnerID=8YFLogxK
U2 - 10.31768/2312-8852.2017.39(4):286-290
DO - 10.31768/2312-8852.2017.39(4):286-290
M3 - Article
C2 - 29284776
AN - SCOPUS:85039958698
SN - 1812-9269
VL - 39
SP - 286
EP - 290
JO - Experimental Oncology
JF - Experimental Oncology
IS - 4
ER -
