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[Expression Changes of Serum Transferrin Receptor and Its Mechanism in Children with Acute Leukemia]

She-An Chen1, Wen-Bin Zhang2

  • 1Department of Clinical Laboratorial Examination, Foshan first people's Hospital, Foshan 528000, Guangdong Province,China.E-mail：chenshean56@163.com.

Zhongguo Shi Yan Xue Ye Xue Za Zhi
|December 4, 2018
PubMed

Insights

Serum transferrin receptor (sTFR) levels are elevated in children with acute leukemia (AL). Downregulating transferrin receptor (TFR) gene expression inhibits leukemia cell proliferation and division, offering a potential therapeutic strategy for AL.

Area of Science:

  • Hematology
  • Molecular Biology
  • Oncology

Background:

  • Acute leukemia (AL) is a significant health concern in children.
  • Serum transferrin receptor (sTFR) is a marker associated with cell proliferation and iron metabolism.
  • Understanding the role of sTFR in pediatric AL is crucial for developing targeted therapies.

Purpose of the Study:

  • To investigate the expression changes of serum transferrin receptor (sTFR) in children with acute leukemia (AL).
  • To explore the mechanism underlying sTFR expression in AL.
  • To evaluate the effect of transferrin receptor (TFR) gene silencing on leukemia cell proliferation and cell cycle.

Main Methods:

  • Comparative analysis of sTFR levels in pediatric AL patients and healthy controls.
  • Detection of TFR mRNA and protein expression in peripheral blood leukemic cells.
  • RNA interference (siRNA) to silence TFR genes in leukemia cell lines (KG-1a and TCHu147).
  • MTT assay and flow cytometry to assess cell proliferation and cell cycle distribution.
  • Western blot to analyze cyclin levels post-TFR gene silencing.

Main Results:

  • Children with AL exhibited significantly higher sTFR levels compared to healthy controls.
  • Elevated TFR mRNA and protein expression were observed in leukemic cells from AL patients.
  • sTFR levels correlated with white blood cell count, leukemic cell burden, hepcidin levels, and risk grade in AL patients.
  • TFR gene silencing significantly inhibited the proliferation of KG-1a and TCHu147 cells.
  • Flow cytometry revealed an increased G0/G1 phase cell ratio and a decreased G2/M phase cell ratio in TFR-silenced leukemia cells.

Conclusions:

  • Peripheral blood leukemic cells in AL patients synthesize increased TFR protein, leading to elevated sTFR levels.
  • Downregulating TFR gene expression effectively interferes with leukemia cell division.
  • Targeting TFR presents a promising therapeutic strategy for pediatric acute leukemia.
Abstract

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