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

A. Matveeva, L. Kovalevska, I. Kholodnyuk, T. Ivanivskaya, E. Kashuba

Research output: Contribution to journalArticlepeer-review

5 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)286-290
Number of pages5
JournalExperimental Oncology
Volume39
Issue number4
DOIs
Publication statusPublished - Dec 2017

Keywords

  • B-cell chronic lymphocytic leukemia
  • SMAD proteins
  • TGFB — SMAD pathway
  • Tumor growth factor beta

Field of Science

  • 3.2 Clinical medicine

Publication Type

  • 1.1. Scientific article indexed in Web of Science and/or Scopus database

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