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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...

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Andrographolide Induces ROS-dependent Apoptosis and Suppresses STAT3 Phosphorylation in Primary Effusion Lymphoma

Itnarin Mongkon1,2, Ryusho Kariya1,3, Phorutai Pearngam1,4

  • 1Division of Hematopoiesis, Joint Research Center for Human Retrovirus Infection and Graduate School of Medical Sciences, Kumamoto University, Kumamoto, Japan.

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Summary

Andrographolide (AG) effectively inhibits primary effusion lymphoma (PEL) cell growth by triggering apoptosis through reactive oxygen species (ROS) and caspase activation, offering a potential new treatment for this aggressive cancer.

Keywords:
PELPrimary effusion lymphomaSTAT3 phosphorylationandrographolideapoptosisreactive oxygen species

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Area of Science:

  • Oncology
  • Pharmacology
  • Cell Biology

Background:

  • Primary effusion lymphoma (PEL) is an aggressive non-Hodgkin lymphoma (NHL) with poor prognosis.
  • PEL exhibits resistance to conventional chemotherapy treatments.
  • Andrographolide (AG), from *Andrographis paniculata*, shows anti-tumor potential but its effect on PEL is unstudied.

Purpose of the Study:

  • To investigate the anti-tumor effects of Andrographolide (AG) on primary effusion lymphoma (PEL).
  • To elucidate the mechanisms underlying AG's action, including apoptosis, reactive oxygen species (ROS), and STAT3 signaling.
  • To evaluate AG's efficacy and safety in a preclinical *in vivo* model.

Main Methods:

  • PEL cell viability assessed by MTT assay; apoptosis evaluated via Annexin V/PI staining and caspase activation.
  • Reactive oxygen species (ROS) generation measured by DCFH-DA staining; protein expression analyzed by Western blotting.
  • Cells co-treated with ROS scavenger (NAC) or caspase inhibitor (Q-VD-OPh); *in vivo* efficacy tested in a xenograft mouse model.

Main Results:

  • AG inhibited PEL cell proliferation dose- and time-dependently.
  • Apoptosis induction was mediated by ROS production and caspase activation.
  • AG suppressed STAT3 phosphorylation in a ROS-dependent manner and reduced tumor burden *in vivo* without toxicity.

Conclusions:

  • AG demonstrates anti-tumor activity against PEL by inducing ROS-dependent apoptosis and inhibiting STAT3 signaling.
  • These findings highlight AG's potential as a novel therapeutic agent for primary effusion lymphoma.
  • Further research into AG for PEL treatment is warranted based on its efficacy and safety profile.