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Related Experiment Video

Updated: Jun 26, 2025

Author Spotlight: Exploring the Role of Inflammation in the Co-occurrence of Primary Sjogren's Syndrome and Lung Adenocarcinoma
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LEPR/FOS/JUNB signaling pathway contributes to chronic restraint stress-induced tumor proliferation.

Jian Zhu1, Qing Liu2, Shuang Nie2

  • 1School of Chemistry and Chemical Engineering, Shanghai University of Engineering Science, 333 Longteng Road, Shanghai, 201620, China; Department of Naval Nutrition and Food Hygiene, Naval Medical University, Shanghai, 200433, China.

Biochemical and Biophysical Research Communications
|May 18, 2024
PubMed
Summary
This summary is machine-generated.

Chronic stress accelerates tumor growth by activating the norepinephrine (NE)-leptin receptor (LEPR) pathway. This pathway involves FOS and JUNB, promoting cancer cell survival and proliferation, highlighting a new mechanism for stress-induced tumor development.

Keywords:
Chronic restraint stressLeptin receptorLiver cancerNorepinephrine

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Area of Science:

  • Oncology
  • Neuroscience
  • Molecular Biology

Background:

  • Psychosocial stress is linked to tumor development.
  • Chronic stress increases norepinephrine (NE) and leptin receptor (LEPR) expression, promoting tumor invasion, metastasis, and proliferation.
  • The precise mechanism of chronic stress-induced tumor proliferation is not fully understood.

Purpose of the Study:

  • To investigate the effect of chronic stress on tumor proliferation.
  • To elucidate the molecular pathways involved in chronic stress-induced tumor growth.

Main Methods:

  • Establishment of subcutaneous tumor models with chronic restraint stress (CRS).
  • Analysis of transcriptomics data from liver cancer patients.
  • In vitro verification of target pathways using cell cultures and gene silencing.

Main Results:

  • CRS significantly increased tumor size compared to controls.
  • CRS elevated mRNA levels of LEPR, FOS, and JUNB in tumor tissues.
  • Norepinephrine (NE) enhanced cancer cell survival and LEPR-FOS-JUNB expression in vitro; LEPR silencing reduced cell viability.

Conclusions:

  • Chronic restraint stress (CRS) activates the LEPR-FOS-JUNB signaling pathway via NE, exacerbating tumor development.
  • This study provides a mechanistic basis for understanding tumor progression under chronic stress conditions.