Increased galectin-3 facilitates leukemia cell survival from apoptotic stimuli

Yi-Lin Cheng, Wei-Ching Huang, Chia-Ling Chen, Cheng-Chieh Tsai, Chi-Yun Wang, Wei-Hsin Chiu, Yuh-Ling Chen, Yee-Shin Lin, Chuan-Fa Chang, Chiou Feng Lin

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29 引文 斯高帕斯(Scopus)


Galectin-3 is regulated for cancer cell survival and apoptosis depending upon the cell type and stimulus. We investigated a glycogen synthase kinase (GSK)-3β/galectin-3-regulated mechanism used by leukemia cells to escape from apoptotic stimuli. Galectin-3 expression was time- and transcription-dependently deregulated in K562 chronic myeloid leukemia cells stimulated for apoptosis by cisplatin (a platinum-based chemotherapy drug), sphingolipid ceramide analog C2-ceramide, and LY294002 (a phosphatidylinositol 3-kinase inhibitor). Notably, galectin-3 was upregulated in survival cells. Forced galectin-3 expression caused resistance to apoptosis, whereas knockdown galectin-3 expression increased susceptibility to apoptosis. Sub-cellular distribution of inducible galectin-3 was mitochondria-specific. Apoptotic stimuli decreased pro-survival Bcl-2 family protein expression (especially Mcl-1), whereas galectin-3 overexpression reversed but it was enhanced by a galectin-3 expression knockdown. Under apoptotic stimulation, GSK-3β was activated after Akt was inactivated and GSK-3β was inhibited-either pharmacologically or using short hairpin RNA to abolish galectin-3, increase apoptosis, and inhibit colony formation-which suggests a pro-survival role for GSK-3β. We found that GSK-3β upregulated galectin-3 and stabilized anti-apoptotic Bcl-2 family proteins, which is important for the escape of leukemia cells from apoptotic stimuli.
頁(從 - 到)334-340
期刊Biochemical and Biophysical Research Communications
出版狀態已發佈 - 8月 26 2011

ASJC Scopus subject areas

  • 生物物理學
  • 生物化學
  • 分子生物學
  • 細胞生物學


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