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Expression of survivin gene in apoptosis induced by dexamethasone in CEM cells

Li He1, Yun-Peng Liu, Ke-Zuo Hou

  • 1Department of Pediatrics, First Hospital of China Medical University, Shenyang 110001, China. hlcmu@yahoo.com.cn

Zhongguo Dang Dai Er Ke Za Zhi = Chinese Journal of Contemporary Pediatrics
|June 22, 2006
PubMed
Abstract

Insights

Dexamethasone (Dex) induces apoptosis in acute lymphoblastic leukemia (ALL) cells by downregulating survivin expression. This finding sheds light on glucocorticoid-induced cell death mechanisms in T-lineage ALL.

Area of Science:

  • Molecular Biology
  • Cancer Research
  • Cell Death Mechanisms

Background:

  • Glucocorticoids are used to treat T-lineage acute lymphoblastic leukemia (ALL).
  • The precise mechanism of glucocorticoid-induced apoptosis remains unclear.
  • Survivin, an inhibitor of apoptosis protein, is implicated in cancer cell survival and drug resistance.

Purpose of the Study:

  • To investigate the role of survivin gene expression in dexamethasone (Dex)-induced apoptosis.
  • To examine the effect of Dex on survivin levels in the human T-lineage ALL cell line, CEM-WT.

Main Methods:

  • CEM-WT cells were treated with varying concentrations of Dex (0.1–10 microM).
  • Cell viability, apoptosis, and survivin protein/mRNA expression were assessed using trypan blue exclusion, flow cytometry, Western Blot, and RT-PCR.
  • Time-course analysis was performed at 24, 48, and 72 hours post-treatment.

Main Results:

  • Dexamethasone significantly inhibited CEM cell growth in a dose- and time-dependent manner.
  • Dex treatment (≥ 5 microM) induced apoptosis, with percentages increasing over time.
  • Survivin protein and mRNA expression were significantly downregulated following Dex treatment.

Conclusions:

  • Dexamethasone-induced apoptosis in CEM cells is closely associated with the downregulation of survivin expression.
  • This study elucidates a key molecular mechanism in glucocorticoid-mediated cancer cell death.

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