The TGF-beta — SMAD pathway is inactivated in cronic lymphocytic leukemia cells

• Published in: Experimental Oncology
• Date: 2017
• ISSN: 1812-9269
• Main Authors: Matveeva, A., Kovalevska, L., Kholodnyuk, I., Ivanivskaya, T., Kashuba, E.
• Format: Article
• Language: English
• Published: Інститут експериментальної патології, онкології і радіобіології ім. Р.Є. Кавецького НАН України 2017
• Subjects: Original contributions
• Online Access: https://nasplib.isofts.kiev.ua/handle/123456789/138586
• Journal Title: Digital Library of Periodicals of National Academy of Sciences of Ukraine
• Cite this: The TGF-beta — SMAD pathway is inactivated in cronic lymphocytic leukemia cells / A. Matveeva, L. Kovalevska, I. Kholodnyuk, T. Ivanivskaya, E. Kashuba // Experimental Oncology. — 2017 — Т. 39, № 4. — С. 286–290. — Бібліогр.: 26 назв. — англ.

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. Objects and Methods: 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.