Skip to main content
padlock icon - secure page this page is secure

Ik6 expression provides a new strategy for the therapy of acute lymphoblastic leukemia

Buy Article:

$42.00 + tax (Refund Policy)

Our previous study demonstrated that the dominant-negative Ikaros isoform 6 (Ik6) is overexpressed in Chinese children with newly diagnosed B-acute lymphoblastic leukemia (B-ALL) and is strongly associated with a poor outcome. The purpose of the present study was to further explore the function of Ik6 in B-ALL. The association between Ik6 expression as detected by real-time PCR and efficacy of chemotherapy was evaluated. The effect of the alteration in Ik6 on leukemic cell lines was assessed by in vitro gain-of-function and loss-of-function techniques. PCR analysis showed that Ik6 expression was decreased when patients completed induction chemotherapy and reached complete remission. Ik6 expression was significantly increased when patients suffered relapse. Stable transfection of Ik6 into the Nalm-6 cell line revealed that Ik6 enhanced proliferation of Nalm-6 cells through the promotion of G0/G1-to-S-phase transition and enhanced chemoresistance to chemotherapeutics through anti-apoptotic effects. However, Ik6 expression did not affect the invasion of Nalm-6 cells. In contrast, silencing of Ik6 in Sup-B15 cells significantly inhibited proliferation and increased chemosensitivity. The present study suggests that Ik6 may be a biological marker of chemosensitivity and relapse and Ik6 may provide a potential therapeutic strategy for ALL.
No Reference information available - sign in for access.
No Citation information available - sign in for access.
No Supplementary Data.
No Article Media
No Metrics

Document Type: Research Article

Affiliations: Department of Pediatrics, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei 430022, P.R. China

Publication date: March 1, 2014

More about this publication?
  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
X
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more