Human lactoferrin upregulates BCL-3 in the K562 erythroleukemia cell

Byungtak Kim, Ho Gun Chang, Sun Jung Kim

Research output: Contribution to journalArticlepeer-review

Abstract

Lactoferrin (LF) plays pivotal roles in primary defense against microbial infection and other cellular processing including immuno-modulation and growth stimulation of cells. To understand the molecular mechanism of LF action we stably overexpressed LF in the K562 erythroleukemia cells and examined differential gene expression using a cDNA microarray. One of the genes that were highly upregulated in the LF-overexpressing cells was the IκB family member B cell lymphoma-3 (BCL-3) that is implicated to promote B cell proliferation and chronic lymphocytic leukemia. Northern blot as well as RT-PCR analysis confirmed that BCL-3 was highly induced in LF-transfected cells. Furthermore, by treating the K562 cells with natural LF protein, we observed a significant increase of BCL-3 messages with the peak at 50 μg/mL and 2 h after treatment. These results suggest that LF signals to induce BCL-3 and thereby promotes B cell proliferation and survival.

Original languageEnglish
Pages (from-to)362-368
Number of pages7
JournalBiochip Journal
Volume5
Issue number4
DOIs
StatePublished - Dec 2011

Keywords

  • B cell
  • BCL-3
  • K562
  • Lactoferrin
  • Leukemia

Fingerprint

Dive into the research topics of 'Human lactoferrin upregulates BCL-3 in the K562 erythroleukemia cell'. Together they form a unique fingerprint.

Cite this