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Targeted Cancer Therapies02:57

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The targeted cancer therapies, also known as “molecular targeted therapies,” take advantage of the molecular and genetic differences between the cancer cells and the normal cells. It needs a thorough understanding of the cancer cells to develop drugs that can target specific molecular aspects that drive the growth, progression, and spread of cancer cells without affecting the growth and survival of other normal cells in the body.
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  1. Home
  3. Celecoxib As A Potential Treatment For Hepatocellular Carcinoma In Populations Exposed To High Pfas Levels.
  1. Home
  3. Celecoxib As A Potential Treatment For Hepatocellular Carcinoma In Populations Exposed To High Pfas Levels.

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Celecoxib as a potential treatment for hepatocellular carcinoma in populations exposed to high PFAS levels.

Boshi Sun1, Yuqiao Zhao1, Shifeng Yang1

  • 1Department of General Surgery, The 2nd Affiliated Hospital of Harbin Medical University, No. 148 BaoJian-ro, Harbin, Heilongjiang Province 150086, China.

Journal of Hazardous Materials
|February 16, 2025

View abstract on PubMed

Summary
This summary is machine-generated.

Per- and polyfluoroalkyl substances (PFAS) exposure significantly increased hepatocellular carcinoma (HCC) progression by upregulating prostaglandin E2 (PGE2). Celecoxib, a PGE2 inhibitor, reduced HCC malignancy and tumor growth in mice.

Keywords:
CelecoxibHepatocellular carcinomaPFASPI3K/AKT pathway

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Area of Science:

  • Environmental Toxicology
  • Oncology
  • Metabolomics

Background:

  • Per- and polyfluoroalkyl substances (PFAS) are linked to adverse health outcomes.
  • Limited research exists on the impact of PFAS mixtures on hepatocellular carcinoma (HCC).

Purpose of the Study:

  • To investigate the effects of PFAS mixtures on HCC cell proliferation, migration, and invasion.
  • To elucidate the underlying mechanisms of PFAS-induced HCC progression.

Main Methods:

  • In vitro studies using JHH-7 and Li-7 HCC cell lines.
  • High-coverage untargeted metabolomics.
  • In vivo mouse models.
  • Pharmacological inhibition of prostaglandin E2 (PGE2) using celecoxib.

Main Results:

  • A 5 μM PFAS mixture significantly enhanced HCC cell malignant progression in vitro.
  • Metabolomic analysis revealed prostaglandin E2 (PGE2) upregulation as a key mediator.
  • Celecoxib treatment reduced PGE2 levels, inhibited HCC cell migration and invasion, and decreased tumor volume in mice.
  • PFAS-induced HCC malignancy is mediated through the PI3K/AKT pathway via increased PGE2 production.

Conclusions:

  • PFAS mixtures accelerate HCC proliferation and invasion.
  • Celecoxib shows potential as a therapeutic agent to inhibit PFAS-induced HCC progression.