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Leptin and its receptor in glucose metabolism of T-cell lymphoma

Tian-Jie Han1,2, Hong-Zhi Xu1, Jun-Shan Li3

  • 1Department of Hematology, Shandong Provincial Hospital, Shandong University, Jinan, Shandong 250021, P.R. China.

Oncology Letters
|October 19, 2018
PubMed

Insights

Leptin and its receptor (ObR) play a key role in T-cell lymphoma (TCL) glucose metabolism. Leptin boosts glucose uptake and cell viability in TCL by promoting glucose transporter 1 (Glut1) expression via ObR.

Area of Science:

  • Oncology
  • Metabolic Research
  • Immunology

Background:

  • T-cell lymphoma (TCL) presents heterogeneous disorders with limited treatment efficacy.
  • Identifying novel therapeutic targets is crucial for improving TCL patient outcomes.
  • Leptin signaling's role in cancer metabolism warrants further investigation.

Purpose of the Study:

  • To investigate the impact of leptin and its receptor (ObR) on glucose metabolism in T-cell lymphoma.
  • To determine the association between ObR expression and glucose transporter (Glut) expression in TCL.
  • To elucidate the mechanism by which leptin influences glucose uptake and cell viability in TCL.

Main Methods:

  • Immunohistochemical analysis of ObR, Glut1, and Glut4 expression in TCL and reactive lymphoid hyperplasia (RLH) tissues.
  • In vitro studies using the human TCL MOLT-3 cell line.
  • Treatment with leptin and ObR-specific small interfering RNA (siRNA) to assess effects on glucose uptake and cell viability.

Main Results:

  • Significantly higher ObR expression was observed in TCL tissues compared to RLH tissues (58.3% vs. 22.2%, P=0.012).
  • ObR overexpression in TCL tissues correlated with high Glut1 expression (P=0.007).
  • Leptin treatment increased glucose uptake and Glut1 expression/recruitment in MOLT-3 cells, an effect reversed by ObR-specific siRNA.
  • Leptin enhanced MOLT-3 cell viability, an effect also abolished by ObR-specific siRNA.

Conclusions:

  • Leptin signaling through its receptor (ObR) is implicated in regulating glucose uptake in T-cell lymphoma.
  • Leptin promotes glucose uptake and cell viability in TCL, potentially via Glut1.
  • ObR represents a potential therapeutic target for modulating glucose metabolism in TCL.
Keywords:
T-cell lymphomaglucose transporter 1glucose uptakeleptinleptin receptor

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