Related Experiment Video

Updated: May 23, 2025

Enhancing Tumor Content through Tumor Macrodissection
10:04

Enhancing Tumor Content through Tumor Macrodissection

Published on: February 12, 2022

9.7K

Luteolin inhibits diffuse large B-cell lymphoma cell growth through the JAK2/STAT3 signaling pathway

Xin-Zhuo Zhan1,2, Yi-Wen Bo3, Yu Zhang4

  • 1Department of Hematology, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, China.

Frontiers in Pharmacology
|March 7, 2025
PubMed

Insights

Luteolin, a natural flavonoid, effectively inhibits diffuse large B-cell lymphoma (DLBCL) growth by inducing apoptosis and cell cycle arrest. It targets the JAK2/STAT3 pathway, showing potential as a novel DLBCL therapeutic agent.

Area of Science:

  • Biochemistry
  • Pharmacology
  • Oncology

Background:

  • Luteolin, a flavonoid from natural sources, exhibits anticancer effects but its mechanism in diffuse large B-cell lymphoma (DLBCL) is not fully understood.
  • Diffuse large B-cell lymphoma (DLBCL) is an aggressive non-Hodgkin lymphoma with unmet therapeutic needs.

Purpose of the Study:

  • To investigate the molecular mechanisms of luteolin as a potential treatment for DLBCL.
  • To evaluate the efficacy of luteolin in preclinical models of DLBCL.
  • To explore the role of the JAK2/STAT3 signaling pathway in luteolin's anti-DLBCL activity.

Main Methods:

  • In vitro studies using human DLBCL cell lines (U2932, OCI-LY10) to assess cell proliferation, apoptosis, and cell cycle.
  • In vivo experiments using a DLBCL tumor xenograft mouse model to evaluate antitumor effects.
  • Molecular dynamics simulations to analyze luteolin's interaction with JAK2.
  • Western blot analysis to examine JAK2/STAT3 pathway protein expression.

Main Results:

  • Luteolin significantly inhibited DLBCL cell proliferation, induced apoptosis, and caused G2/M cell cycle arrest.
  • In vivo administration of luteolin suppressed tumor growth in mice.
  • Luteolin treatment downregulated phosphorylated JAK2 and STAT3 levels in DLBCL cells and tumors.
  • Computational analysis confirmed stable binding between luteolin and JAK2.

Conclusions:

  • Luteolin demonstrates significant anti-DLBCL activity through the inhibition of the JAK2/STAT3 signaling pathway.
  • Luteolin represents a promising therapeutic candidate for DLBCL treatment.
  • Targeting the JAK2/STAT3 pathway with luteolin warrants further clinical investigation for DLBCL.
Keywords:
Janus kinase 2/signal transducer and activator of transcription 3diffuse large B-cell lymphomaluteolinmechanismtraditional Chinese medcine

More Related Videos

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries08:49

Identification of Mediators of T-cell Receptor Signaling via the Screening of Chemical Inhibitor Libraries

Published on: January 22, 2019

9.1K
Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity07:09

Myeloid Innate Signaling Pathway Regulation by MALT1 Paracaspase Activity

Published on: January 7, 2019

7.4K

Related Concept Videos

The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
8.6K
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
5.9K
Receptor Downregulation in MVBs01:15

Receptor Downregulation in MVBs

Multivesicular bodies (MVBs) are mature endosomes that sort ubiquitinated proteins and then fuse with lysosomes to degrade the sorted proteins. Epidermal growth factor (EGF) and its receptor (EGFR) form a complex that can be internalized through endocytosis, sorted into an MVB, and later degraded.
The EGFR can initiate signaling pathways that  lead to cell proliferation, migration, and differentiation. Overexpression of EGFR  stimulates cells to proliferate. Excessive  EGFR...
2.0K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

The orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
4.6K