Galectin-12 inhibits granulocytic differentiation of human NB4 promyelocytic leukemia cells while promoting lipogenesis

Huiting Xue, Ri Yao Yang, Guihua Tai, Fu-Tong Liu

Research output: Contribution to journalArticlepeer-review

11 Scopus citations


As a member of the galectin family of animal lectins, galectin-12 is preferentially expressed in adipocytes and leukocytes. In adipocytes, galectin-12 is associated with lipid droplets and regulates lipid metabolism and energy balance, whereas its role in leukocytes is not clear. Analysis of galectin-12 expression in a public data set of acute myeloid leukemia (AML) samples revealed that it is selectively overexpressed in the M3 subtype, which is also known as acute promyelocytic leukemia (APL). To investigate the role of galectin-12 in APL cells, we manipulated its expression in the APL cell line, NB4, and measured resultant effects on all-trans-retinoic acid (ATRA)-induced granulocytic differentiation. With a doxycycline-inducible gene knockdown system, we found that suppression of galectin-12 promoted ATRAinduced neutrophil differentiation but inhibited lipid droplet formation. Our results indicate that overexpression of galectin-12 contributes to a differentiation block in APL cells, and suppression of galectin-12 facilitates granulocytic differentiation. Furthermore, these data suggest that lipogenesis and other aspects of myeloid differentiation can be differentially regulated. Taken together, these findings suggest that galectin-12 may be a target for treatment of the ATRA-resistant subset of APL.

Original languageEnglish (US)
Pages (from-to)657-664
Number of pages8
JournalJournal of Leukocyte Biology
Issue number4
StatePublished - Oct 1 2016


  • Acute myeloid leukemia
  • Acute promyelocytic leukemia
  • Lipid droplets
  • Myeloid differentiation
  • PPARγ

ASJC Scopus subject areas

  • Immunology
  • Cell Biology


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