Cancer Chemotherapy and Pharmacology

, Volume 65, Issue 6, pp 1039–1046 | Cite as

LLL-3, a STAT3 inhibitor, represses BCR-ABL-positive cell proliferation, activates apoptosis and improves the effects of Imatinib mesylate

  • Andre Luiz Mencalha
  • B. Du Rocher
  • D. Salles
  • R. Binato
  • E. Abdelhay
Original Article



The chimeric protein BCR-ABL, a constitutively active protein-tyrosine kinase, triggers downstream signalling proteins, such as STAT3, ultimately resulting in the survival of myeloid progenitors in BCR-ABL-positive leukemias. Here, we evaluated the effect of LLL-3, an inhibitor of STAT3 activity, on cell viability and its addictive effects with Imatinib mesylate (IM) treatment in BCR-ABL-positive cells.


Viability of cell lines was determined using the WST-1 assay in response to drug treatment, either LLL-3 alone or in conjunction with IM. Annexin V-FITC/PI staining, sub-G1 DNA content and Caspase-3/7 activation assays were performed to evaluate apoptosis.


LLL-3 treatment decreased cell viability, triggered apoptosis and activated Caspases-3/7 in K562 cells. LLL-3 increases IM treatment to inhibited cell viability and activation of apoptosis in BCR-ABL-positive cell lines.


LLL-3 reduced cell viability and induced apoptosis in K562 cells. Moreover, the observed addictive effects of co-treatment with IM and LLL-3 suggest this combination has therapeutic potential.


LLL-3 STAT3 BCR-ABL Imatinib 


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Copyright information

© Springer-Verlag 2009

Authors and Affiliations

  • Andre Luiz Mencalha
    • 1
    • 2
  • B. Du Rocher
    • 1
    • 2
  • D. Salles
    • 1
    • 2
  • R. Binato
    • 2
  • E. Abdelhay
    • 2
  1. 1.Instituto de Biofísica Carlos Chagas Filho, CCS, UFRJRio de JaneiroBrazil
  2. 2.Laboratório de Células-tronco, Divisão de laboratórios do CEMOInstituto Nacional do Câncer (INCa)Rio de JaneiroBrazil

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