Investigating the Role of JAK/STAT Pathway on Dasatinib-Induced Apoptosis for CML Cell Model K562

Ceyda Tunakan Dalgıç; Burçin Tezcanlı Kaymaz; Melda Cömert Özkan; Ayşegül Dalmızrak; Fahri Şahin; Güray Saydam

doi:10.1016/j.clml.2015.02.012

Investigating the Role of JAK/STAT Pathway on Dasatinib-Induced Apoptosis for CML Cell Model K562

Clin Lymphoma Myeloma Leuk. 2015 Jun:15 Suppl:S161-6. doi: 10.1016/j.clml.2015.02.012.

Authors

Ceyda Tunakan Dalgıç¹, Burçin Tezcanlı Kaymaz², Melda Cömert Özkan³, Ayşegül Dalmızrak², Fahri Şahin³, Güray Saydam³

Affiliations

¹ Department of Internal Medicine, Ege University Medical Faculty, İzmir, Turkey. Electronic address: dr_ceydat@yahoo.com.
² Department of Medical Biology, Ege University Medical Faculty, İzmir, Turkey.
³ Department of Hematology, Ege University Medical Faculty, İzmir, Turkey.

PMID: 26297271
DOI: 10.1016/j.clml.2015.02.012

Abstract

We aimed to evaluate the cytotoxic and apoptotic effects of dasatinib (BMS-354825) on K562 chronic myeloid leukemia (CML) cells and to examine the roles of STAT genes on dasatinib-induced apoptosis. The results showed that dasatinib decreased proliferation and induced apoptosis in K562 cells in a dose- and time-dependent manner. mRNA and protein levels of STAT5A and STAT5B genes were significantly reduced in dasatinib-treated K562 cells. These data indicated that STAT inhibition by dasatinib might be therapeutic in JAK/STAT pathway-associated malignancies after confirmation with clinical studies.

Keywords: Apoptosis; Chronic myeloid leukemia; Dasatinib; JAK/STAT pathway; STAT5.

Publication types

Review

MeSH terms

Apoptosis / drug effects*
Dasatinib / therapeutic use*
Humans
Leukemia, Myelogenous, Chronic, BCR-ABL Positive / drug therapy*
STAT5 Transcription Factor
Signal Transduction
Tumor Suppressor Proteins

Substances

STAT5 Transcription Factor
STAT5A protein, human
Tumor Suppressor Proteins
Dasatinib